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

16 Perianal Hidradenitis Suppurativa
277
is usually good. There are typically some differences in the color and texture of the graft after
healing compared with surrounding skin. Skin
grafts may be placed on granulated wounds with
no signs of infection, though some also place
them directly after excision. Compared with secondary intention, skin grafting has a shorter time
to closure but may be more uncomfortable during
healing and mobility may be limited to allow for
the graft to heal.
A variety of local advancement, rotational, and
free soft tissue aps can be used to reconstruct HS
wounds. Flap surgery, however, may be technically more difcult to perform, more invasive, and
have the potential for failure when compared to
secondary healing or skin grafting. Flap coverage
should be strongly considered when HS debridement results in areas of exposed nervous, vascular, or skeletal structures (e.g. tendons, bones).
One factor in surgical planning is that the size of
the defect is often underestimated preoperatively
so the ap needs to be large enough for adequate
coverage [32]. Complex ap reconstruction is
most benecial when planned in advance in conjunction with a soft tissue surgical expert, such
as a plastic surgeon. Recurrence rates following
primary healing, ap, and skin grafting were
noted to be 15%, 8%, and 6%, respectively [38].
A combined approach of several surgical
modalities may be required for complex HS. A
combination of incisional drainage, un-roong,
debridement, and primary and secondary intention is often used for complex cases. For large,
extensive areas of disease, staged excision is often
employed. The authors prefer to divide areas of
HS disease into functional anatomic regions and
address each separately, with an eye on preserving anatomic function for the treatment duration.
For instance, a patient with bilateral perianal,
perineal, and inguinal disease may be treated
with four smaller staged debridements, with each
debridement addressing a quadrant of active disease (right inguinal, left inguinal, left anal margin,
right anal margin) whereby preserving relatively
normal function in the remaining three quadrants.
Such staged strategies allow a patient to rest or
weight-bear on healed (or yet- to- be treated) tissue
until the active surgical area heals.
Rarely, a diverting stoma may be sought
prior to extensive debridements to theoretically decrease bacterial contamination of healing wounds. Commonly, plastic surgeons may
request temporary fecal diversion prior to perianal skin grafting or complex healing of extensive perineal wounds. Although temporary fecal
diversion makes putative sense for severe perianal
HS awaiting complex reconstruction, the benets
of diversion remain controversial. As has been
reported anecdotally for small series of necrotizing perianal soft tissue infections, conscientious
and careful perianal wound care with tube-based
fecal management systems may facilitate wound
healing without a stoma [40].
Special consideration should be paid to
patients with concomitant CD and HS with regard
to surgery. If infra-inguinal HS is felt to be arising from stulizing perianal disease a combined
approach of medical and surgical management is
often required. If extensive perianal HS can be
attributed to a solitary stula-in-ano, wide local
cutaneous debridement plus seton control of the
stula can be performed. Complicated stulas,
anal stenosis, or refractory mucosal inammation may require proctectomy in association with
cutaneous debridement.
Squamous Cell Carcinoma
Squamous cell carcinoma is a rare but serious complication of HS that typically occurs
after long periods of uncontrolled inammation [41]. The pattern of development is similar
to Marjolin’s ulcers in burns and carcinoma of
stulous tracts in CD. Though there are only a
total of 86 cases reported in the literature [42],
one cohort study demonstrated a prevalence of
4.6% [43]. SCC is more common in males and in
patients with gluteal, perianal, or perineal disease
affecting large areas. The median time from diagnosis of HS is 20–30years [41]. The treatment
is wide local excision, and postoperative radiotherapy has been used for regional lymph nodes
or unresectable disease due to proximity to sensitive neurovascular structures [44]. The mortality
rate is up to 50% in some series [41].

278
E. Steinhagen and M. F. McGee
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Hemorrhoidal Disease
DavidE.Beck
17
Introduction
Hemorrhoids and the symptoms they produce
have plagued mankind throughout recorded
history [1]. In the Bible, the Old Testament of 1
Samuel, Chaps. 5 and 6 describe the Philistines
after taking the Ark of the Covenant from the
Israelis as being smitten by god with aphelim or
techorim. Both words are believed by scholars to
relate to hemorrhoids [2, 3]. Many centuries ago
Maimonides described a variety of soothing
medications, ointments, and even suppositories for
the treatment of hemorrhoids and argued against
surgery as a treatment for the condition [4].
The term hemorrhoid has, from the patient’s perspective, always signied a variety of anal complaints varying from minor itching to acute disabling
pain. As the presence of some hemorrhoidal tissue
is normal, hemorrhoidal disease should be thought
of as hemorrhoidal tissue that causes signicant
symptomatology. Large sums of money are spent
on products to control these symptoms, and the
amount of work lost because of hemorrhoids is economically important [5]. Our understanding of etiology and symptoms helps us to make
recommendations for therapy. This chapter
discusses the anatomy, pathophysiology, and
methods of treatment of symptomatic hemorrhoids.
D. E. Beck (*)
Department of Colon and Rectal Surgery,
Ochsner Clinic, New Orleans, LA, USA
Anatomy
Hemorrhoids are cushions of vascular tissue found
in the anal canal [2]. Hemorrhoidal tissue is present
at birth and in nonpathologic conditions.
Microscopically, this tissue contains vascular structures whose walls do not contain muscle. Thus
hemorrhoids are not veins (which have muscular
walls) but are sinusoids (Fig. 17.1) [6]. Studies
have also demonstrated that hemorrhoidal bleeding
is arterial and not venous. When these sinusoids are
injured (disrupted), hemorrhage occurs from presinusoidal arterioles. The arterial nature of the bleeding explains why hemorrhoidal hemorrhage is
bright red and has an arterial pH [7].
Cutaneous sensation in the perianal area is
mediated through the pudendal nerve and the
sacral plexus, both arising from sacral nerve roots
2 through 4, as described in Chap. 1. Some of the
pressure sensation in this area may also be mediated by sacral nerve endings (S-2 to S-4) located
in the lower rectum and pelvic oor [5].
In humans, hemorrhoidal tissue is thought
to contribute to anal continence by forming a
spongy bolster, which cushions the anal canal
and prevents damage to the sphincter mechanism
during defecation [2]. In addition, this tissue acts
as a compressible lining which allows the anus
to close completely. The three main cushions (or
bundles) lie at the left lateral, right anterolateral,
and right posterolateral portion of the anal canal.
Smaller secondary cushions may occasionally
© Springer International Publishing AG, part of Springer Nature 2019
D. E. Beck et al. (eds.), Fundamentals of Anorectal Surgery,
https://doi.org/10.1007/978-3-319-65966-4_17
281

282
ac
Vein
Internal
Hemorrhoid
Dentate
Line
Sinusoid
Vascular
Space
Arteriole
b
External
Hemorrhoid
Separate
D. E. Beck
Combined
Fig. 17.1 Hemorrhoidal anatomy. (a) Arteriovenous
anastomosis (AV shunts) forming hemorrhoidal plexus.
(b) Fourth degree hemorrhoids. (c) Usual position of the
lie between these main cushions. Each bundle
starts superiorly (cranially) in the anal canal and
extends inferiorly (caudally) to the anal margin.
The superior portion of the hemorrhoidal tissue (above the dentate line) is covered by anal
mucosa and the inferior portion (below the dentate line) is covered by anoderm or skin.
hemorrhoids. Separate external and internal hemorrhoids
are seen on the left and a combined internal-external
hemorrhoidal complex is seen on the right
prolonged straining, pregnancy, and derangement of the internal sphincter [2]. Constipation
and the associated straining with defecation as
suggested by Burkitt and Graham-Stewart [8]
are related to eating habits, specically, to a
low-residue diet. The typical American low ber
diet may explain the high prevalence of constipation, straining, and hemorrhoidal symptoms
in America [9]. With time (aging) the anatomic
Pathophysiology
structures supporting the muscularis submucosae
weaken which leads to slippage or prolapsation
Etiology
of the hemorrhoidal tissue. Haas etal. conrmed
microscopically that anal supporting tissues dete-
Enlargement or pathologic changes in hemorrhoidal tissue result in symptoms of the
“hemorrhoidal syndrome.” Proposed etiologic
factors for these changes include constipation,
riorate by the third decade of life [10]. Finally,
several authors have demonstrated that patients
with hemorrhoids have increased activity of the
internal anal sphincter [11, 12]. In addition to the

17 Hemorrhoidal Disease
283
hemorrhoidal plexuses lying supercial to the
sphincter mechanism, it has been theorized that
a dysfunctional sphincter could lead to venous
outow obstruction and congestion, followed by
engorgement of the hemorrhoids, and subsequent
symptoms [13]. All of these conditions contribute toward stretching and slippage of the hemorrhoidal tissue. The overlying skin or mucosa is
stretched and additional brous and sinusoidal
tissue develops. The extra tissue tends to move
caudally toward the anal verge making it susceptible to injury and causing symptoms to develop.
A survey into the prevalence of benign anorectal
disease demonstrated that 9% of adults had previous treatment of hemorrhoidal disease and 8%
had hemorrhoidal symptoms [14].
Hemorrhoids are not related to portal hypertension [7]. With increased portal venous pressure,
the body develops portosystemic communications in several locations. In the pelvis, communications enlarge between the superior and middle
hemorrhoidal veins which result in development
of rectal varices. These varices are located in
the lower rectum, not the anus. Due to the rectum’s large capacity, they rarely bleed. Older literature suggested a relationship between portal
hypertension and hemorrhoids partly due to the
fact that hemorrhoids are common and therefore
many portal hypertensive patients will have hemorrhoids. If portal hypertension was an etiologic
factor, hemorrhoidal bleeding would be venous
blood rather than arterial bleeding as described
above. Hemorrhoidal symptoms may be difcult
to manage in patients with portal hypertension as
their liver disease frequently is associated with
coagulation and platelet problems.
pain. Symptoms from external hemorrhoids usually result from thrombosis of the hemorrhoidal
plexus. The rapid tissue expansion produced by
the clots and edema causes pain. Physical effort
is felt to be an etiologic factor in thrombosis of
external hemorrhoids. Physical examination
reveals one or more tender blue colored masses
at the anus; additional symptoms are discussed
below.
Internal hemorrhoids are located proximal (cranial) to the dentate line and covered by
columnar mucosa or transitional epithelium.
Based on size and clinical symptoms, internal
hemorrhoids can be further subdivided by Grades
[2, 15]. Grade 1 hemorrhoids protrude into, but
do not prolapse out of the anal canal. Grade 2
hemorrhoids prolapse out of the anal canal with
bowel movements or straining, but spontaneously reduce. Grade 3 hemorrhoids prolapse
during the maneuvers described above and must
be manually reduced by the patient. Grade 4
hemorrhoids are prolapsed out of the anus and
cannot be reduced (Fig. 17.1b). Hemorrhoids
that remain prolapsed may develop ischemia,
thrombosis, or gangrene. Patients may have both
internal and external hemorrhoids (mixed or
combined) (Figs.17.1c and 17.2).
Classication
For anatomic and clinical reasons hemorrhoidal
tissue has been divided into two types: External
and Internal. External hemorrhoids are located
in the distal one third of the anal canal (distal to
the dentate line) and are covered by anoderm
(modied squamous epithelium that bears no
skin appendages) or skin (Fig. 17.1a). As this
overlying tissue is innervated by somatic nerves,
it is sensitive to touch, temperature, stretch, and
Fig. 17.2 Prolapsed thrombosed internal hemorrhoids
that have caused swelling of the external hemorrhoids as
well

284
D. E. Beck
Evaluation
Symptoms
Patients with any anal complaints commonly
present to physicians complaining of “hemorrhoids.” Careful exploration of their symptoms
will often lead to the correct diagnosis.
Symptoms associated with hemorrhoidal disease include: mucosal protrusion, pain, bleeding,
a sensation of incomplete evacuation, mucous
discharge, difculties with perianal hygiene, and
cosmetic deformity. General disorders of bowel
function such as diarrhea and constipation, and
associated disorders such as bleeding problems
should be considered. A dietary and medication
history should always be taken.
Except when thrombosis or edema occurs,
hemorrhoids are painless. Painless bleeding occurs
from internal hemorrhoids, is usually bright red,
and is associated with bowel movements. The
blood will occasionally drip into the commode and
stain the toilet water bright red. After trauma by
rm stools or forceful bowel movements, bleeding
may continue to occur with bowel movements for
several days. The bleeding will often then resolve
for a variable period of time. It is unusual for
hemorrhoidal bleeding to be severe enough to
cause anemia but has been reported to occur in 0.5
patients per 100,000 population [16].
Prolapse may be appreciated by the patient as
an anal mass, a feeling of incomplete evacuation,
or a mucous discharge. The patient’s requirement
to manually reduce prolapsed hemorrhoids
should be ascertained. If thrombosis or gangrene
occurs, it will be apparent on physical examination and may be associated with systemic
symptoms.
modied left lateral decubitus (Sims) position
(Fig. 2.1) is an acceptable alternative. Inspection
of the anus should be done slowly, with calm
reassurance by the examiner. The skin about the
perianum, genitalia, and sacrococcygeal areas
should be scrutinized. Gentle, steady spreading
of the buttocks will allow for close inspection of
the majority of the squamous portion of the anal
canal.
Digital examination gives the examiner an
appreciation for the amount and location of any
pain in the anal canal. It enables assessment of
the sphincter tone and helps exclude other diseases such as palpable tumors or abscesses in the
lower rectum and anal canal. Hemorrhoids are
not generally palpable unless quite large or
thrombosed.
Anoscopy, usually done with a side-viewing
instrument, permits visualization of the condition of the anoderm and internal hemorrhoidal
complexes. As the patient strains, the hemorrhoids bulge into the lumen of the anoscope. The
degree of prolapse may be assessed by gently
withdrawing the anoscope as the patient strains.
Rigid proctosigmoidoscopy and exible sigmoidoscopy form an important part of the initial examination and are performed to exclude
more proximal disease. If the patient is less
than 40 years old and hemorrhoidal disease
compatible with symptoms is seen on physical
examination, most authors feel that no additional work-up is required. If the patient is older
than 40, hemorrhoidal disease is not observed,
or additional symptoms are present, a barium
enema or colonoscopy is obtained to identify
other etiologies for bleeding not observed by
the proctoscopy.
Examination
Examination of the anal area is usually undertaken with the patient in a prone position on a
special proctologic table. If the patient is elderly
or uncomfortable in this position, however, the
Dierential Diagnosis
It is extremely important that other causes of
bleeding, itching, or discharge be considered as
listed in Table17.1. Although patients invariably
attribute anal pain to hemorrhoids, acute anal
pain is almost always caused by either anal s-

17 Hemorrhoidal Disease
Table 17.1 Differential diagnosis in hemorrhoidal disease
Symptoms Other diseases Hemorrhoidal problems
Acute pain Fissure
Abscess/stula
Chronic pain Fissure
Abscess/stula
Perianal Crohn’s disease
Bleeding Fissure
Colorectal polyp
Colorectal cancer
Itching/discharge Hypertrophic anal papilla
Fistula
Condylomata (anal warts)
Rectal prolapse
Anal incontinence
Lump or mass Hypertrophic anal papilla
Abscess
Anal tag
Crohn’s disease
Unusual Anal or rectal tumor (benign or malignant)
Ulcerative colitis
Thrombosed
Prolapsed thrombosed
Internal hemorrhoid
Thrombosed external hemorrhoid
Prolapse
Thrombosed
Prolapsed
285
sure or anorectal abscess. Pain from hemorrhoids
occurs only in association with thrombosis or
prolapse.
Treatment
General Principles
Treatments are many and varied with some treatments, as described earlier, dating back to biblical times [17]. Modern therapy includes
identication and correction of gastrointestinal
(GI) tract dysfunction, minimization of symptoms, and in some patients, correction of anal
abnormalities, excision of excess hemorrhoidal
tissue and prevention of slippage or prolapse.
Treatment can be nonoperative or operative.
Nonoperative techniques include dietary modications, topical medications and measures (such
as Sitz baths) to reduce symptoms. Operative
techniques, many of which can be performed in
an ofce setting, include tissue xation, major
tissue excision, or physiologic alterations of the
anal canal (Lord dilation or lateral internal
sphincterotomy). The method chosen is usually
related to the type of hemorrhoidal tissue causing
symptoms, and the experience and judgment of
the treating physician [2].
Internal Hemorrhoids
Diet andStool Bulking Agents
Dietary modication is a mainstay for any therapy for hemorrhoidal disease [17]. If the patient
is constipated or straining, a diet high in ber
(usually at least 20–30g/day) is recommended,
striving for a soft, formed compressible stool that
is easy to pass. This type of stool reduces the
requirement to strain with bowel movements and
lessens the chance of hemorrhoidal injury.
Moesgaard and colleagues [18] conducted a prospective double-blind trial, which demonstrated
that psyllium ber, when added to the diet of
patients with anal bleeding and pain with defecation, improved their symptoms over a 6-week
period. Patients with diarrhea and hemorrhoidal
disease, after an evaluation of the underlying
cause of their loose stools, should also receive
dietary manipulation with ber and antidiarrheals
as indicated.

286
Table 17.2 Fiber products
Type of ber Dosage (g) Trade name Manufacturer
Bran
Psyllium 3.5 Metamucil™ Procter & Gamble, Cincinnati, OH
6.0 Konsyl™ Konsyl Pharmaceuticals, Fort Worth, TX
Methylcellulose 1–3 Citrucel™ Merrell Dow Pharmaceuticals, Cincinnati, OH
Calcium
Polycarbophil
1–3 Fibercon™ Lederle Laboratories American Cyanamid Co, Pearl
1–3 Konsyl™ Fiber
Tablets
River, NY
Konsyl Pharmaceuticals, Fort Worth, TX
D. E. Beck
Table 17.3 Treatment of internal hemorrhoids by degree
of prolapse
Severity Treatment
First degree
(no prolapse)
Second degree
(spontaneously
reducible)
Third degree (manual
reduction necessary)
Fourth degree
(irreducible)
Acutely prolapsed
and thrombosed
a
Excisional hemorrhoidectomy is recommended if exter-
nal tags are also present
Dietary
Infrared coagulation OR
banding, or sclerotherapy
Dietary
Plus banding OR infrared
coagulation, or sclerotherapy
Dietary
Plus banding OR infrared
coagulation, or sclerotherapy
OR
Excisional
hemorrhoidectomy
Excisional hemorrhoidectomy
Rarely, multiple rubber band
ligations
Emergency
hemorrhoidectomy
a
Dietary ber is more appropriately referred to
as a stool normalizer rather than a stool softener.
It is uncommon for dietary ber to cause complications, and allergic reactions to the active or
inactive ingredients are exceptionally rare. The
most common clinical difculty is non-compliance due to problems with taste or symptoms of
bloating and crampy abdominal pain. Fiber products currently available are listed in Table17.2.
Manufacturers have attempted to improve the
palatability of these products in several ways.
Adding avoring and sweeteners has improved
taste but usually at a higher cost and less ber per
unit volume. The different ber sources may produce variable effects in different patients. It is
advisable, therefore, to try alternate products if
the rst selection does not produce the desired
results. To minimize symptoms, many providers
nd it helpful to start patients at a lower dose of
the ber supplement and to slowly increase the
amount of ber ingested until the desired stool
consistency is achieved. It is also important to
counsel patients to ingest an appropriate amount
of water with their ber; generally 80–120 oz.
(240–360 mL) per day. Fiber consumption of
greater than 35 g/day with inadequate water
intake can predispose to bezoar formation.
Polyethylene glycol (PEG) supplementation (e.g.
Miralax, Bayer Health Care, Whippany, NJ) aids
in the retention of water in the stool. It can be
helpful in patients that are less compliant with
ber especially females. If dietary manipulations
fail to relieve symptoms, additional therapy is
indicated (Table17.3).
Flavonoids
Flavonoids are plant products that have been prescribed to reduce hemorrhoidal bleeding. A metaanalysis of 14 randomized trials (1514 patients)
found limitations in methodological quality, heterogeneity, and potential publication bias [19].
The authors had questions on the benecial
effects in the treatment of hemorrhoids. These
products have not been used widely in North
America.
Topical Medications andMeasures
Sitz baths, a bidet, or soaks in a warm tub are
used to soothe the acutely painful anal area. Dodi
and associates [20] demonstrated a signicant
reduction in anal pressure after patients with
anorectal disorders soaked in warm (40 °C)

17 Hemorrhoidal Disease
287
water. Soaking time should be limited as
prolonged exposure to water can lead to edema of
the perineal skin and subsequent pruritus. Some
patients prefer to apply ice packs to the anal area.
Again, as long as contact is not prolonged, this
option is acceptable if it reduces symptoms.
The pharmaceutical industry has actively promoted multiple products such as creams, foams,
and suppositories. One per cent hydrocortisone
may temporally reduce the symptoms caused by
pruritus associated with hemorrhoidal disease.
However, prolonged use of topical steroids may
attenuate the skin, predisposing it to further
injury. Suppositories, after insertion, end up in
the lower rectum rather than in the anal canal
where hemorrhoids are located. Outside of
providing a little lubrication of the stool, they
have little to no pharmacologic rationale in the
management of hemorrhoidal disease [21].
Ointments can cause or exacerbate pruritus ani,
and again except for those that contain a topical
anesthetic (e.g. 1% pramoxine hydrochloride)
offer little benet except for thrombosed external
hemorrhoids. Success in reducing symptoms
associated with thrombosed external hemorrhoids has also been reported with topical nitro-
glycerin [20]. Effective marketing of over the
counter medications, the placebo effect of any
medication placed on the bothersome area, and
the intermittent nature of hemorrhoidal symptoms explain the large volumes of these products
purchased in the United States.
Rubber Band Ligation
Rubber band ligation was originally described by
Blaisdell in 1958 [22] and subsequently rened
and popularized by Barron in 1963 [23]. Placement
of a tight rubber band around excess hemorrhoidal
tissue constricts the blood supply to the contained
tissue, which sloughs over 5–7days. This leaves a
small ulcer, which heals xing the tissue to the
underlying muscle. Due to its simplicity, safety
and effectiveness, rubber band ligation is currently
the most widely used technique in the United
States for treating rst, second and some third
degree internal hemorrhoids [5].
To accomplish this procedure, informed consent is obtained and an anoscope is inserted into
the anus (the author prefers a slotted lighted
scope) (Fig.17.3e). A hemorrhoid bundle is identied and through the anoscope, a band is placed
using one of two types of ligators (Fig. 17.3).
Fig. 17.3 Hemorrhoidal
banders. (a) Band
ligator(McGivney type).
(b) Band loaders.
(c)Avascular clamp.
(d)Suction ligator
(McGown).
(e)Fiberoptic anoscope.
(f)Rubber bands (From
Beck DE.Hemorrhoids.
In Beck DE. (ed)
Handbook of Colorectal
Surgery. 3rd ed. JP
Medical, London, 2013.
With permission)
a
b
d
c
e
f
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