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AccessSurgery | Print: Chapter 3. Anatomy and Physiology
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where C = compliance, = stool viscosity, L = length of anal canal, P
max
= maximal pressure, r = radius of anal canal, and
V
rectum
= volume in rectum.
Continence is achieved if the formula returns a true solution when the patient's data are entered. Hence, continence is
directly correlated with compliance, viscosity (or firmness), length of anal canal, and maximal pressure but inversely
correlated with anorectal diameter.
Control and Coordination
Fecal and urinary control is acquired in the first 2–4 years of life: the term incontinence is therefore only applicable to the
time after unless morphologic defects are obviously preventing development of control (eg, meningomyelocele, etc).
Control occurs subconsciously even at sleep, reinforced through conscious contraction on demand.
Examples and Symptoms of Dysfunction
Plug: sphincter defect, sphincter dysfunction, anal disconfiguration:
– Absent puborectalis function
complete incontinence
– Deficient EAS
impaired voluntary control
– Deficient IAS
impaired fine tuning
– Keyhole deformity
seepage
Reservoir: decreased volume after LAR, pelvic radiation, tumors, stricture, ongoing inflammation.
Stool quality: diarrhea, IBS, IBD, radiation proctitis.
Associated Pathology
Pelvic floor dysfunction.
Pelvic organ prolapse syndrome.
Obstetric/surgical trauma.
Associated Problems
Functional incontinence absence of any measurable or visible deficiency.
Cross-Reference
Anophysiology studies (Ch. 2)
Fecal incontinence (787.6) (Ch. 4)
CARCINOGENESIS
Overview
Tumor: abnormal growth or mass of cells no longer linked to physiologic function or demand.
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Cancer: characteristic growth patterns:
Invasiveness: disrespect of tissue boundaries invasion of other structures.
Size-dependent potential to metastasize: access to blood/lymph vessels or other structures tumor spread to
distant locations.
Cancer is a genetic disease: series of mutations that result in a growth advantage: (a) germline mutation
transmission to
the next generation (inherited defect); (b) somatic mutation (more common) spontaneous mutation during tissue/organ
growth, development, and maintenance.
Elements
GATEKEEPER GENES (ONCOGENES/TUMOR-SUPPRESSOR GENES)
APC gene (adenoma-polyposis coli, 5q): tumor-suppressor gene control of cell-to-cell adhesions and intercellular
communication; found in 60% of even small adenomatous polyps and carcinomas
early event in carcinogenesis.
MCC gene (mutated in colon cancer): tumor supressor gene
K-ras (12p): normal function in intracellular signal transduction and stimulated cell division; found in larger
adenomas and carcinomas
stimulates cell growth.
DCC (deleted in colon cancer, 18q): tumor-suppressor gene progression from benign polyp toward malignant
growth.
p53 (17p): tumor-suppressor gene among most frequent gene mutations in human cancers late event in the
development of the invasive phenotype.
CARETAKER GENES
Mismatch repair genes: hMLH1, hMSH2, hMSH6, PMS1, PMS2 encode proteins for repair of nucleotide mismatches.
Microsatellites: stretches in the DNA with several-fold repetition of a short sequence of 1–5 nucleotides
microsatellite instability: loss or gain of repeat units in germline
microsatellite allele: found in 15% of sporadic
colorectal cancer, in > 90–95% of HNPCC.
Physiologic Sequence
Normal cell division: multiplication of cells as defined by tissue demand: once demand is satisfied increased
production is redirected to maintenance production to uphold steady state.
Normal cell cycle: high number of spontaneous gene mutations without biologic or growth advantage repair
mechanism or inherent suicide program (apoptosis, if cell damage too severe).
Pathophysiology
Adenoma-Carcinoma Model (Vogelstein, 1988): colorectal tumorigenesis as multistep process related to accumulation
of genetic events
uninhibited cell growth proliferation and clonal expansion.
Carcinogenesis: several independent accidents failure to recognize and correct DNA damage continued
replication
accumulation of faulty gene products within cell survival advantage proliferative response:
GR
tumor
– DR
tumor
> GR
normal
– DR
normal
[GR = growth rate, DR = death rate]
DNA mismatch repair (MMR) systems:
– Cell division: DNA duplication with original DNA serving as template for replicated copy, DNA polymerase
serves as proofreader recognition of mismatch genes halt to DNA synthesis and removal of defective
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sequence.
– Failure of DNA mismatch repair system
development of mutations.
– Increased proliferation
increased genetic instability malignant cells without feedback-controlled growth
regulation.
Two types of genetic instability:
– Chromosome level: loss of chromosomal material, ie, chromosomal instability (CIN), asymmetric chromosome
distribution (mitosis) gel electrophoresis with loss of one or more bands = loss of heterozygosity (LOH).
– DNA level: replication errors in repetitive short polymorphisms
additional band or bands = microsatellite
instability (MSI).
Examples and Symptoms of Dysfunction
FAP: APC gene mutation 5q21
Attenuated FAP (AFAP): APC gene mutation in proximal 5'-end, exon 9, or distal 3'-end fewer polyps, later age for
cancer, more proximal polyp distribution.
HNPCC: defective mismatch repair genes.
Associated Pathology
Extracolonic pathology (eg, desmoid tumors): more frequent with distal APC gene mutations.
Associated Problems
Accelerated carcinogenesis in HNPCC: adenoma-carcinoma sequence shortened to 2–3 years (vs 8–10 years in
sporadic colorectal cancer)
earlier screening, shorter interval.
Genetic testing.
Cross-Reference
Polyps (211.3) (Ch. 4)
Polyposis syndromes (211.3, 235.2) (Ch. 4)
Familial adenomatosis polyposis (FAP; 211.3, 235.2, V84.09) (Ch. 4)
Hereditary nonpolyposis colon cancer (HNPCC, 153.8, V84.09) (Ch. 4)
Colorectal cancer—colon cancer (153.X) (Ch. 4)
Amsterdam II criteria for HNPCC (App. 2)
Bethesda criteria for MSI testing (App. 2)
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McGraw-Hill Manual: Colorectal Surgery > Chapter 4. Diseases and Problems >
ANAL FISSURE (565.0)
Overview
Anal fissures are frequent, simple to diagnose, and often overlooked. A fissure is a longitudinal tear/wound/ulceration
between the dentate line and the anal verge, typically located in the midline, associated with high anal sphincter tone. Risk
factors: constipation, chronic diarrhea (idiopathic, IBD, post–gastric bypass), but fissure may also occur with normal bowel
movements.
Acute fissure is defined as new onset, no signs of chronicity, typically related to identifiable acute episode of
constipation or diarrhea.
Chronic fissure is defined as either > 3 months of symptoms or morphologic signs of chronicity (elevated/indurated
wound edges, exposed sphincter muscle, sentinel skin tag, hypertrophic anal papilla).
Complications are rare: development of a perirectal fistula/abscess, chronic pain (even if fissure healed), ie, anismus.
Pathophysiology: acute or chronic stress/trauma to the anal canal (constipation, diarrhea) results in superficial tear; acute
fissure will heal in 40–60% with appropriate improved stool management, or may turn into chronic anal fissure and result in
a vicious circle: increasing sphincter tone, hypertonicity of internal anal sphincter muscle (resting tone)
fissure hiding
between anal canal folding such that it cannot clean out pain increased sphincter spasm etc.
Treatment of fissure aims at normalizing stool regularity and decreasing sphincter tone.
Epidemiology
Exact prevalence and incidence are unknown (referral bias); in a specialist clinic, 3–5% of patients have a fissure as
presenting symptom. More common in young and middle-aged adult patients; most frequent cause of rectal bleeding in
children.
Symptoms
Patients often present with "painful hemorrhoids" as they feel the sentinel skin tag and notice the pain during and after
bowel movements.
Pain: typically post defecation, varying degrees, ranging from mild itching to discomfort to massive excruciating pain periods.
But an estimated 10% of patients do not complain of pain, or they just have pruritus or mild discomfort.
Duration of pain: typically during and post bowel movements, occasionally several hours thereafter, or permanent/constant
pain.
Bleeding: acute fissure—sometimes significant bright red bleeding; chronic fissure—more often just traces of blood on toilet
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paper. Severe hemorrhage or anemia unlikely related to fissure.
Lump: "irritated" external hemorrhoids (sentinel skin tag), but absence of dynamic protrusion during bowel movement.
Differential Diagnosis
Pain: thrombosed external hemorrhoid, abscess, levator ani spasm, anismus.
HIV-associated ulcer: HIV infection+; ulceration: often in the same location and/or eccentric; sphincter tone typically not
increased, or even decreased.
Crohn disease: anal symptoms may be the only manifestation or be associated with other signs/locations of active Crohn
disease.
STDs: syphilis, herpes.
Perirectal fistula/abscess: particularly horseshoe fistula characteristically originates from posterior midline.
Tuberculosis: clinical suspicion, atypical presentation, associated pulmonary symptoms, positive PPD test.
Malignancy-associated lesion: cancer, melanoma, leukemia, lymphoma, plasmocytoma.
Pathology
Epithelial ulceration, unspecific acute and chronic infiltrates.
Evaluation
REQUIRED MINIMAL STANDARD
History: onset/pattern of symptoms, reversible prolapse or persistent "lump," bowel habits, preexisting incontinence?
Clinical examination:
External inspection (skin tags, thrombosed external hemorrhoid, erythema/induration)? Lateral traction to the
buttocks
exposure of posterior and anterior midline: often sufficient to diagnose the fissure (Figure 4–1). If fissure
confirmed and significant pain reported, digital exam or instrumentation at the first presentation is not indicated!
External palpation: tight sphincter tone, hypertonic internal sphincter muscle with well-palpable intersphincteric
groove.
Figure 4–1.
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Chronic anal fissure with and without sentinel skin tag.
Full/partial colonic evaluation as per general screening guidelines (if history and findings consistent: may be deferred for 3–4
weeks until acute symptoms controlled).
ADDITIONAL TESTS (OPTIONAL)
Anoscopy/proctoscopy: rule out tumor, hemorrhoids, proctitis, etc; if fissure is confirmed, these exams are only indicated if
there are inconsistencies of complaints and findings!
Atypical (eccentric) fissures: cultures, biopsy.
Classification
Acute vs chronic anal fissure.
NONOPERATIVE TREATMENT
Improving stool regularity (increased supplemental fibers, increased fluid intake, stool softener, temporary mild laxative).
Sitz baths: to help patient relax, to wash off area.
Chemical sphincterotomy:
Topical 0.2% nitroglycerin ointment (fingertip amount applied to anal verge twice daily): 40–60% chance of healing
fissure within 4–8 weeks; side effects: headaches (particularly in the beginning, may respond to acetaminophen),
tachycardia. Contraindicated with concomitant sildenafil (Viagra): risk of malignant arrhythmias. If no
improvement/healing in 4–8 weeks, or significant side effects
Botox.
Topical 2% diltiazem or 0.2% nifedipine ointment: applied twice or three times per day to anal verge; same cure
rate as NTG, less headache, but local irritation may occur.
Injection of Botox into internal anal sphincter muscle: local disinfection and injection of 10–20 units of botulinum
toxin A (suspended in 1 mL 0.9% NaCl) directly into internal anal sphincter muscle on each side (total amount: 20–40
units): estimated 80–85% chance of curing the fissure within 6–12 weeks; may repeat one time.
Operative Treatment
INDICATION
Severe acute symptoms: surgery by far providing the fastest relief.
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Failure of nonoperative management (including pharmacologic sphincterotomy).
OPERATIVE APPROACH
Lateral internal sphincterotomy (gold standard): 95% cure, 5(–15)% incontinence to stool or gas (often recovering
within 1 year).
Lateral internal sphincterotomy with excision of fissure and sentinel skin tag: indicated if fissure is very deep and/or
hiding underneath a large redundant sentinel skin tag.
Fissurectomy alone in combination with injection of Botox, potentially with external skin flap: in patients in whom
weakening of the sphincter should be avoided (preexisting incontinence, chronic diarrhea, status post gastric bypass,
IBD with potential need for future IPAA).
Obsolete procedure: manual anal dilation; uncontrolled dilation results not only in stretching of the internal sphincter
muscle but also of the external sphincter muscle
high risk of fecal incontinence. Possible renaissance of concept with
use of controlled dilatation?
Comment: fissurectomy and sphincterotomy in the area of the ulcer/fissure
risk of keyhole deformity, generally better to
perform sphincterotomy through separate lateral incision.
Outcome
Combined efforts should result in 95–100% of healing. Benchmark: < 10% problems with fecal control, rapid ability to return
to workforce.
Follow-Up
Recheck patient after 4–6 weeks of initiated treatment. Order appropriate tests (eg, cultures/biopsies) if no response or
atypical presentation. Once resolved, no specific follow-up needed.
Cross-Reference
Pain, perirectal (Ch. 1)
Pelvic muscles (Ch. 3)
Lateral internal sphincterotomy (LIS) (Ch. 5)
ANAL SKIN TAGS (455.9)
Overview
Skin tags represent focal redundancy of the perianal skin. They may be solitary or form excessive changes of the anal
landscape with deep troughs, hence causing a potential problem for local hygiene. Uncomplicated skin tags may develop
spontaneously or result from known episodes of thrombosed external hemorrhoids. Sentinel skin tags result from a
persistent chronic problem (eg, chronic anal fissure). Most commonly, anal skin tags have no disease character and, if a
problem, are more a cosmetic/emotional one.
Epidemiology
Prevalence: very frequent, statistics unavailable/unreliable.
Symptoms
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Most commonly asymptomatic. Occasionally negative interference with local hygiene.
Occasionally itching/irritation or "painful hemorrhoid"
high index of suspicion that chronic fissure is hiding underneath.
Differential Diagnosis
Sentinel skin tags (with underlying chronic anal fissure).
External hemorrhoid (visible vascular component with continuum to internal hemorrhoids).
Condylomata.
Tumor (malignant, benign).
Pathology
Squamous cell epithelium covering paucicellular stroma (eg, minimal inflammatory elements).
Evaluation
REQUIRED MINIMAL STANDARD
History: patient to define the actual problem: constant vs dynamic presence, need for reduction, associated symptoms
(bleeding, pain, itching etc), daily bowel habits, constipation? Previous colonic screening?
Clinical examination: anal configuration (location and number of skin tags)? Underlying pathology (fissure, fistula,
hemorrhoids, rectal prolapse)? Sphincter tone?
Anoscopy/proctoscopy: tumor, hemorrhoids, proctitis, etc.
Full/partial colonic evaluation: not because of the tag as such but as indicated per general screening guidelines.
Classification
Uncomplicated skin tag.
Symptomatic skin tag: sentinel skin tag, irritated skin tag.
Nonoperative Treatment
No treatment needed for uncomplicated skin tag.
Treatment of underlying fissure in sentinel skin tag.
Operative Treatment
INDICATION
Patient desire to have skin tag removed (no medical necessity).
Patient desire to improve local hygiene (medically justifiable for extensive tags).
Sentinel skin tag in treatment-refractory anal fissure.
OPERATIVE APPROACH
Simple excision (office vs OR setting).
Fissure: sphincterotomy alone vs sphincterotomy with fissurectomy and excision of skin tag.
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Outcome
In patients bothered aesthetically by the presence of a skin tag: low success rate of talking them out of a medically
unnecessary surgical excision.
Follow-Up
None for uncomplicated skin tag.
Cross-Reference
Lump or mass (Ch. 1)
Anal fissure (565.0) (Ch. 4)
Hemorrhoids (455.X) (Ch. 4)
Pruritus ani (698.0) (Ch. 4)
Anal condylomata (078.10) (Ch. 4)
HEMORRHOIDS (455.X)
Overview
"Hemorrhoids" remain the most common colorectal complaint; however, a majority of patients associate any type of
anorectal symptoms with "hemorrhoids" even though they do not necessarily have a hemorrhoid problem. "Hemorrhoidal
cushions" are a component of normal anal anatomy and contribute to physiologic continence mechanism. Anatomic primary
locations: right anterior, right posterior, left lateral.
Hemorrhoidal disease: pathologic engorgement of submucosal vascular plexus, often asymptomatic, increasingly resulting in
bleeding (superficial erosions), progressive prolapse, less commonly, pain. Contributing factors: constipation with straining,
diarrhea, pregnancy, familial clustering, age.
Important distinction between internal/mixed hemorrhoids and external hemorrhoids (Figure 4–2A).
Figure 4–2A.
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External hemorrhoid component.
Appropriate hemorrhoid treatment depends on (1) a correct clinical diagnosis that rules out alternative differential diagnoses,
(2) the patient's type and severity of symptoms, and (3) the grade, extent, and location of the hemorrhoid at the time of
presentation.
Special circumstances: pregnancy, HIV infection, IBD, liver disease.
(Note: liver cirrhosis is not associated with increased incidence of hemorrhoids but may result in rectal varices!)
Epidemiology
Prevalence: 3–6%; peak age: between 45 and 65 years, unusual before adolescence; approximately one-third of patients
will seek medical treatment.
Symptoms
Internal hemorrhoids: bleeding and dynamic prolapse associated with bowel movement. Other symptoms generally
unspecific: pain/discomfort (only when partially thrombosed or incarcerated [grade IV, Figure 4–2B]), itching (from
moisture).
Figure 4–2B.