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CLINICAL

jaHNA.CRAie-^AD
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CIBA

V O L U M E 37

CLINICAL
SYMPOSIA

A
NUMBER 6

1985

Anorectal Disorders
Koherl D Fry, MD
Ira ] Kodner MD
lllustrated by ]ohn A. Craig, MD
Edited by Mara
Erdlyi-Brown

0^ o

Anorectal A n a t o m y

C o m m o n Anorectal Disorders

Hemorrhoids

A n a l Fissure

10

Anorectal Abscess a n d Fstula i n A n o

13

Perianal Hidradenitis Suppurativa

16

Rectovaginal Fstula

17

A n a l Incontinence

20

Rectal Prolapse

22

Fecal Impaction

24

Pruritus A n i .

24

Sexually Transmitted Anorectal Disease

Dro, Sania 'VMSa Xspm


CIRUJANA PROCTOLOGA
MSPL.l''0"Fol.2N'>. 6
3200279

26

Condylomata A c u m i n a t a

26

C h l a m y d i a l Infections

28

Gonorrhea

28

Syphilis

30

Herpes

30

Perianal a n d A n a l Neoplasms

30

Neoplasms of the A n a l M a r g i n

31

Neoplasms of the A n a l Canal

31

Milton N Donin, PhD Editorial


Diredor
Maria Erdlyi-Brown, Managing Editor

CLINICAL SYMPOSIA IS published for the medical profession

by ihe Pharmaceuticals Divisin,


CIBA-GEIGY
Corporation, Summit, New Jersey 07901
Address all correspondence lo Medical Education,
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COPYRIGHT 1985 PHARMACEUTICALS DIVISION,
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Anorectal Disorders
ROBERT

D FRY,

MD

IRA

] KODNER,

MD

]ewish Hospital at Washington University


Medical Center
Assistant Professor of Clinical Surgery
Washington University School of Medicine
St. Louis, Missouri

Jewish Hospital at Washington University


Medical Center
Assistant Professor of Clinical Surgery
Washington University School of Medicine
St. Louis, Missouri

Disease is very od and nothing about it has changed.

The anorectal ring, 1.0 to 1.5 cm above the


dentate line, is the u p p e r border of the anal
sphincteric complex and is easily palpable b y
digital examination of the anus.
For anatomists, the anal canal begins at the
dentate line and ends at the anal verge. Surgeons, however, view the anal canal as starting at
the anorectal ring and t e r m i n a t i n g at the anal
verge. In this m o n o g r a p h , the surgeon's concept
of the anal canal prevails.

It is we who change as we learn to recognize what


was formerly imperceptible.

}.M.

Charcot

Disorders of the anus and rectum have tormented m a n k i n d since the very b e g i n n i n g of
recorded history I n 1686, the French royal
surgeon Flix cured K i n g Louis X I V of an anal
fstula b y p e r f o r m i n g a f i s t u l o t o m y Fifteen
generations later, surgeons still treat anal fstulas
w i t h an operation very similar to that p e r f o r m e d
by Flix. Nevertheless, a better u n d e r s t a n d i n g of
anorectal anatomy, physiology, and pathology
has accumulated over these centuries, affording
the contemporary physician a rational treatment
for anorectal disease.
ANORECTAL ANATOMY

I m m e d i a t e l y above the dentate line, the rectal


mucosa has 8 to 14 convoluted l o n g i t u d i n a l
folds, or rectal columns. Each t w o adjacent columns are connected at the dentate line b y an
anal valve, thus creating the anal crypt. Small,
r u d i m e n t a r y anal glands open into some, b u t n o t
all, of the crypts. The anal glands may extend
t h r o u g h the internal sphincter as far as the intersphincteric plae, b u t they do not pentrate the
external sphincter

Basic anatomic landmarks. The alimentary


tract terminates at the funnel-shaped anorectum.
The anorectum comprises the s k i n of the surr o u n d i n g perianal regin, the anal canal, and the
rectum (Pate 1). The anal verge, the dentate line,
and the anorectal r i n g are the three m a i n
anatomic points of reference. The anal verge,
the external b o u n d a r y of the anal canal, is the
j u n c t i o n between the anal and perianal s k i n .
A l t h o u g h the precise border is often indistinct,
anal e p i t h e l i u m lacks hair follicles, sebaceous
glands, or sweat glands f o u n d i n perianal s k i n .

A b o v e the anorectal ring, the lower intestine


dilates to f o r m the rectal ampuUa. P r o m i n e n t
mucosal folds, the rectal valves of H o u s t o n , are
f o u n d w i t h i n the rectum. The lower and u p p e r
valves lie o n the left side of the rectum, and the
m i d d l e valve lies o n the right side. The m i d d l e
rectal valve usually lies at the level of the anterior
peritoneal reflection. Since these valves are not
as t h i c k as the rectal w a l l , they are excellent
biopsy sites.

The dentate line (anorectal line), the cephalad


border of the anal canal, is a true mucocutaneous
j u n c t i o n . It represents the unin of the e m b r y onic ectoderm w i t h the entodermal gut, and it
lies approximately 1.0 to 1.5 cm above the anal
verge. In a transitional zone ( f r o m 6 to 12 m m i n
length), the columnar e p i t h e l i u m of the rectum
changes to cuboidal e p i t h e l i u m , w h i c h joins the
squamous e p i t h e l i u m at the dentate line.

A n a l musculature. The anal canal is surr o u n d e d b y an inner a n d outer muscular tube


(Pate 2). T h e inner muscular tube, the internal
sphincter, is actually a thickened c o n t i n u a t i o n of
the circular smooth muscle s u r r o u n d i n g the rect u m . It is an i n v o l u n t a r y muscle approximately
2.5 cm i n length. The outer muscular tube, the
external sphincter, is a v o l u n t a r y skeletal muscle
d i v i d e d into three partsdeep, superficial, a n d

CLINICAL SYMPOSIA

Pate 1

Anatomy of Anus and Rectum


G e o g r a p h i c anatomy of a n o r e c t u m

Rectosigmoid
junction
Superior
rectal valve
Valves

Middle
rectal valve

Rectal
ampulla

Houston

Inferior
rectal valve
Anorectal
ring
Dentate
line

Anatomic
anal canal
(anoderm)

Surgical
anal canal
JOHNA.CRAIC^AD
)C1BA
1

A n o r e c t a l anatomy

Longitudinal mu
of rectum
Circular muscle
rectum
Muscularis mucosae
Mucosa

Puborectalis
muscle
Rectal columns
Anorectal ring
Infernal hemorrfio
plexus

Deep external
sphincter
Intersphincteric
plae
Infernal sphincter
Anal crypt
Anal gland (lies
intersphincteric
opens into crypt)
Superficial external
sphincter
Dentate line
External hemorrhoidal
plexus
Subcutaneous exte
sphincter

VOLUME 37,

NUMBER 6

Pate 2

Anal Musculature
Puborectalis
muscle

External
sphincter
Deep
portion
Superficial
portion
Subcutaneous
portion

Longitudinal
muscle of rectum

External sphincter
downward continuation
of puborectalis portion
of levator ani

Circular muscle
of rectum

Puborectalis muscle

Intersphincteric
plae

External sphincter
Deep
portion

Downward continuation
and thickening of circular
smooth muscle of rectum
form internal sphincter

Superficial
portion -
Subcutaneous
portion

JOHSA.CRAiq^>D
CIBA

infernal sphincter
sits within external
sphincter like tube
within tube

Infernal
sphincter
inner tube)
External
sphincter
complex
outer tube)

CLINICAL SYMPOSIA

subcutaneous. It is a d o w n w a r d extensin of
the puborectalis; the external sphincter extends
f r o m the puborectalis muscle to slightly below
the internal sphincter at the anal verge.
The superior border of the external sphincter
blends w i t h the puborectalis, a component of the
levator ani. The puborectalis forms a muscular
sling, originating at the pubis and joining behind
the rectum. The puborectalis, upper external
sphincter, and internal sphincter f o r m the palpable anorectal ring.
The intersphincteric plae, the space between
the internal and external sphincters, represents a
fibrous continuation of the longitudinal smooth
muscle layer of the rectum. As mentioned earlier, anal glands that empty into the anal crypts
also extend into the intersphincteric plae.
Nerve supply. The rectum is innervated by
both sympathetic and parasympathetic nerves.
The external sphincter and levator ani muscles
are innervated by the inferior rectal branch of
the internal pudendal nerve (52, S3, S4), as well
as by fibers from the fourth sacral nerve.
The internal sphincter is innervated by bth
sympathetic and parasympathetic nerves. The
sympathetic nerves arise from thoracolumbar
segments, which unite below the inferior mesenteric artery to form the inferior mesenteric
plexus and descend to the superior hypogastric
plexus located just inferior to the aortic b i f u r cation. These purely sympathetic fibers then
bifrcate and descend as the hypogastric nerves.
Anterior and lateral to the rectum, parasympathetic fibers f r o m S2, S3, and S4 (the nervi
erigentes) unite w i t h the hypogastric nerves to
f o r m the inferior hypogastric plexi. M i x e d fibers
f r o m these plexi innervate the prostate, rectum,
bladder, penis, and internal anal sphincter The
sympathetic innervation of the internal sphincter
is motor, while the parasympathetic innervation
is i n h i b i t o r y Injury to the pelvic autonomic
nerves d u r i n g pelvic surgery may result in b l a d der dysfunction, impotence, or both.
Below the dentate line, cutaneous sensations
of heat, cold, pain, and touch are conveyed by
afferent fibers i n the inferior rectal nerves.
Above the dentate line, a poorly defined duU
sensation, experienced when the mucosa is
pinched or internal hemorrhoids are ligated, is
probably carried by parasympathetic fibers.
Vascular s u p p l y The terminal branch of the
inferior mesenteric artery, the superior rectal
artery, descends to the upper rectum in the
sigmoid mesentery It then divides into right and
left branches, w i t h subsequent smaller branches
penetrating the muscular coat of the rectum
VOLUME 37,

NUMBER 6

(Pate 3). The middle rectal arteries arise from


the internal iliac arteries, supplying the lower
rectum and upper anal canal. The inferior rectal
arteries arise from the internal pudendal arteries,
crossing the ischiorectal fossae to supply the anal
sphincter muscles.
Blood returns f r o m the anus by two routes.
Above the dentate line, the internal h e m o r r h o i dal plexus drains into the superior rectal vein
and subsequently into the inferior mesenteric
vein and portal system. Below the dentate line,
the external hemorrhoidal plexus drains into
the internal iliac vein, via the middle rectal vein
or via the pudendal vein, w h i c h receives blood
f r o m the inferior rectal vein.
The l y m p h channels foUow the arterial routes.
L y m p h f r o m the upper and middle rectum
drains into the inferior mesenteric l y m p h nodes.
L y m p h f r o m the lower rectum can also flow to
the inferior mesenteric nodes, or it can flow laterally, cise to the middle rectal arteries, to the
internal iliac nodes.
Lymphatics f r o m the anal canal above the
dentate line flow to the inferior mesenteric
nodes, as well as laterally to the internal iliac
nodes, traversing the ischiorectal fossa. L y m p h
f r o m the anal canal below the dentate line usually flows to the inguinal nodes.
C O M M O N ANORECTAL DISORDERS
Hemorrhoids
A precise definition of hemorrhoids does not
exist because of the considerable controversy
regarding their nature. In the past, hemorrhoids
have been described as varicosities of the
branches of the superior hemorrhoidal veins, but
this is probably an oversimplification.
Recent studies place greater emphasis on the
role of anal "cushions," w h i c h are usually
located in the anal canal above the dentate line
(Pate 4 ) . These cushions consist of three thick,
vascular submucosal bundles that always lie i n
the left lateral, right posterolateral, and right
anterolateral positions. The main function of
these cushions w i t h i n the anal canal is not fully
understood, however, they appear to engorge
w i t h blood d u r i n g defecation, thus protecting
the anal canal f r o m abrasin. The seprate cushions also allow the anus to dilate during defecation. Internal hemorrhoids may result w h e n
these cushions enlarge and descend d o w n w a r d
into the anal canal. Communications exist
between the internal and external hemorrhoidal
plexi, and if the Communications become
enlarged, combined (or mixed) internal and
external hemorrhoids result.

Pate 3

Vascular Supply of Anus and Rectum


V e n o u s return

Portal vein

Blood returns from anus via two routes.


Below dentate line, external fiemorrfioidal
plexus drains into inferior vena cava via
inferior pudendal veins. Above dentate
line, internal hemorrhoidal plexus drains
into portal system via superior rectal vein

Interior mesenteric
vein
Inferior vena cava
Common iliac
vein

JOHNA.CRAie^AD
GIBA

Superior rectal
vein
External
iliac vein
Infernal iliac vein
Infernal hiemorrhoidal
plexus
~ Middle rectal vein

Inferior
mesenteric
artery
Inferior
mesenteric
vein

Inferior rectal vein


External hiemorrhioidal
plexus
Vascular supply

Infernal iliac vein


Infernal iliac artery
Superior rectal
artery
Superior rectal
vein
Middle rectal artery
Middle rectal vein

Infernal pudendal artery


Infernal pudendal vein

Inferior rectal artery


Inferior rectal vein

CLINICAL SYMPOSIA

Pate 4

Hemorrhoids
Left
lateral

Usual position of internal


fiemorrhoids. or anal cushions

Infernal hemorrhoidal plexus


Dentate line
Externa! hemorrhoidal plexus

JOMNACRAiq^^D
CIBA

T y p e s of h e m o r r h o i d s

Origin below
dentate line
(external
plexus)

Origin above
dentate line
(internal
plexus)

Origin above
and below
dentate line
(internal and
external
plexus)

Infernal hemorrhoid
External hemorrhoid
VOLUME 37,

NUMBER 6

Mixed hemorrhoid

Internal hemorrhoids. A l t h o u g h the etiology


is not well understood, internal hemorrhoids are
recognized as symptomatic, enlarged bundles of
vascular tissue located above the dentate line
and covered w i t h rectal mucosa. Since internal
hemorrhoids have no somatic innervation, they
usually present w i t h o u t pain.
Clinical

features and diagnosis.

These hemor-

rhoids are best classified by symptoms. The


major symptoms of internal hemorrhoids are
bleeding and protrusion. The bleeding is bright red
and may be seen i n the stool, on the toilet tissue,
or i n the toilet. Prolapsing internal hemorrhoids
may produce a mucous discharge that causes
itching, but usually these symptoms are due to
other causes. First-degree internal hemorrhoids
bleed b u t do not protrude through the anal orfice. Second-degree internal hemorrhoids protrude
at defecation but reduce spontaneously
Thirddegree internal hemorrhoids protrude and must
be manually replaced i n their anatomic position
above the dentate line. Fourth-degree hemorrhoids protrude permanently and cannot be
reduced manually
It is most important to remember that the
mere presence of hemorrhoids is not necessarily
an indication for treatment. Hemorrhoids should
be treated only to alleviate symptoms; the best
treatment is the least intervention possible to
achieve this goal.
Even though internal hemorrhoids are the
most common source of rectal bleeding, it is
imperative that other causes be excluded. Since
internal hemorrhoids cannot be detected by
digital examination, diagnosis can only be made
by anoscopy It is mandatory that proctosigmoidoscopy be performed to rule out other
sources of bleeding, such as carcinoma or proctitis. The stool at the upper point of the sigmoidoscope should be tested for blood, and if
occult blood is present, b a r i u m enema and perhaps colonoscopy should be done routinely
For patients over 4 5 years of age w i t h rectal
bleeding, a b a r i u m enema is generally recommended to exelude colonic cncer A b a r i u m
enema should accompany, but never replace,
the simple and highly effective proctosigmoidoscopic examination.
Treatment. M i l d symptoms of bleeding and
protrusion can usually be controUed by diet,
bowel regulation, and avoidance of prolonged
straining at the time of defecation. Increasing the
fiber content of the diet w i t h raw vegetables,
fruits, whole grain cereals, and h y d r o p h i l i c
b u l k - f o r m i n g agents (such as p s y l l i u m seed
compounds) can reduce and often alleviate all
8

symptoms. If bleeding and protrusion persist


despite conservative treatment, the hemorrhoids
should be treated surgically
Elastic ligation of the friable redundant h e m orrhoidal tissue is quite satisfactory in most
instances (Pate 5 ) . The procedure is quite simple. The hemorrhoid is visualized through the
anoscope and grasped w i t h frceps. The redundant tissue is pulled into a double-sleeved c y l i n der on which there are two ltex bands. The
bands are discharged from the cylinder, and the
hemorrhoidal bundle is ligated. The necrotia
redundant tissue sloughs off i n 5 to 1 0 days.
Certain precautions, however, must be taken
w i t h this form of treatment. The ligatures must
be placed at least 5 m m above the dentate line to
avoid extreme discomfort. Ideally, the ligatures
should be placed at the level of the anorectal
ring. A b o u t 2 5 % of patients experience m i l d , duU
anal discomfort, lasting for 2 to 3 days foUowing
the procedure. M i l d analgesics and w a r m baths
are usually enough to relieve the discomfort. In
about 1 % of patients, brisk bleeding occurs when
the necrotic tissue sloughs off; electrocautery is
then necessary to stop the hemorrhage. A suction cautery can be very useful i n this instance.
A b o u t 2 % of patients treated w i t h ligation of the
internal hemorrhoid develop thrombosis of an
external h e m o r r h o i d , which may then require
excisin.
The ligation procedure is performed in the
physician's office, w i t h no special preparations
required. Patients w i t h a bleeding diathesis or
w i t h portal hypertension are not good candidates for ligation. Usually only one hemorrhoid
is ligated d u r i n g one procedure; ligation of more
than one bundle has been associated w i t h
increased discomfort, as well as a higher c o m p l i cation rate. Further ligations can be performed
every 4 weeks until all symptoms of bleeding or
prolapse are alleviated.
Most symptoms from internal hemorrhoids
can be successfully treated by diet, bowel regulation, or elastic ligation. Occasionally, however,
large mixed (combined internal/external) h e m orrhoids are not amenable to ligation because
the ligature w o u l d have to incorprate painsensitive tissue at or below the dentate line. In
these cases, an excisional hemorrhoidectomy is
the treatment of cholee.
Sometimes the entire ring of internal hemorrhoidal tissue may be incarcerated outside the
anal canal, resulting i n spasm of the internal
sphincter, massive local edema, and severe pain.
In these instances, injecting the edematous tissue
w i t h a local anesthetic containing epinephrine
CLINICAL SYMPOSIA

Pate 5

Surgical Management of Infernal Hemorrhoids


E l a s t i c ligation techi'^ique

Bands on
inner drum

Elastic bands
on inner drum

Elastic
band

Outer drum
Hemorrhoid grasped by
clamp and pulled through
drums of instrument

Inner drum retracts and releases


bands onto base of hemorrhoid
JOMNACRAiq^AD

Excisin t e c h n i q u e for mixed h e m o r r h o i d s

GIBA

Hemorrhoid grasped
and pulled down

Externa! sphincter

External hemorrhoid dissected freedissection carried cephalad to free


internal portion

Deep suture
ligation of
vascular
pedicle

Infernal
sphincter
VOLUME 37,

NUMBER 6

Dead space
closed with suture
incorporating skin
edges and muscle
9

and hyaluronidase can b r i n g significant relief.


Dissipation of the edema b y m a n u a l compression can also be achieved, a l l o w i n g r e d u c t i o n of
the prolapsed tissue (Pate 6). Elastic ligatures
can t h e n be applied to the r e d u n d a n t i n t e r n a l
h e m o r r h o i d s . The t h r o m b o s e d external h e m o r rhoids, if present, are excised. If m a r k e d spasm
of the i n t e r n a l sphincter is present, an i n t e r n a l
s p h i n c t e r o t o m y is appropriate.
External hemorrhoids. S k i n tags and acutely
t h r o m b o s e d veins are the t w o general categories
of external h e m o r r h o i d disease. S k i n tags are
usually asymptomatic and require no treatment.
O f t e n they are merely the residua of previously
t h r o m b o s e d h e m o r r h o i d s . Edematous, s h i n y
skin tags, however, may be indicative of Crohn's
disease. Occasionally, chronic s k i n tags cause
itching a n d i r r i t a t i o n , these s y m p t o m s s h o u l d be
treated w i t h good anal hygiene and rarely
require excisin.
T h r o m b o s e d external h e m o r r h o i d s appear as
tense l u m p s just outside the anal verge. O n occasion, the s k i n o v e r l y i n g the thrombosis becomes
necrotic, a n d the clot m a y partially a n d spontaneously extrude t h r o u g h this defect. Associated
pain is quite variable. T h e pain is most intense
d u r i n g the first 2 days foUowing thrombosis, and
then it usually subsides r a p i d l y
Treatment. The course of treatment depends
u p o n the patient's s y m p t o m s . W i t h m i n i m a l
tenderness, treatment is not needed. Modrate
tenderness is best treated w i t h analgesics a n d
w a r m soaks. Severe pain requires excisin of the
entire t h r o m b o s e d h e m o r r h o i d , using local anesthesia. Sigmoidoscopy, however, should always
be done p r i o r to excisin. This procedure should
be delayed u n t i l satisfactory local anesthesia has
been established. Because of the very high rate
of recurrence, simple incisin and enucleation of
the clot are inadequate treatment. A f t e r excisin
of the h e m o r r h o i d , the w o u n d is usually closed
but may be left open.
A n a l Fissure
A n a l fissure is an elliptic ulcer i n the anal
canal that usually extends f r o m the dentate line
to the anal verge, o v e r l y i n g the lower half of the
internal sphincter (Pate 7). I n men, the fissure is
almost always located cise to the posterior
m i d l i n e , b u t about 1 % of fissures i n males reside
cise to the anterior m i d l i n e . I n w o m e n , about
80% of fissures are posterior, a n d the remainder
are located anteriorly The precise etiology of
anal fissures has yet to be d e t e r m i n e d . H o w ever, fissures p r o b a b l y are related to tearing
of the a n o d e r m at the time of defecation. T h e
10

Y-shaped divergence of the external sphincter


i n the m i d l i n e m a y offer insufficient support to
the anal canal d u r i n g defecation, c o n t r i b u t i n g to
the f o r m a t i o n of a m i d l i n e fissure d u r i n g the
passage of a large fecal bolus.
C l i n i c a l features and diagnosis. M o s t fissures
are quite superficial a n d heal r a p i d l y A t times,
however, the fissure may be deep and chronic
and is referred to as an " a n a l ulcer " The fibers
of the internal anal sphincter are exposed at the
base of a deep fissure. The s k i n adjacent to a
chronic fissure m a y be edematous, f o r m i n g a
sentinel edematous tag, w h i c h may be mistaken for
a h e m o r r h o i d . I n a d d i t i o n , the anal valve above
the fissure may become enlarged, f o r m i n g a
h y p e r t r o p h i e d anal papilla. Rarely, secondary
infection can also occur, resulting i n a perianal
abscess.
Studies have c o n f i r m e d clinical observations
that chronic anal fissure is associated w i t h
abnormalities of the internal sphincter N o r mally, rectal distensin ( d u r i n g defecation, for
example) is foUowed b y a reflex relaxation of
the i n t e r n a l sphincter I n patients w i t h an anal
fissure, the reflex relaxation is f o l l o w e d b y an
" o v e r s h o o t " contraction. T h i s overshoot contraction may contribute to the c h r o n i c i t y of
the fissure; it disappears foUowing appropriate
treatment.
Secondary fissures m a y be caused b y previous
anal operations that result i n scarring, stenosis,
and loss of a n o d e r m . Individuis w i t h chronic
lose stools, laxative abusers, or patients w h o
have undergone intestinal bypass procedures for
obesity may develop anal stenosis associated
w i t h a fissure. Crohn's disease is a w e l l - k n o w n
cause of anal fissure; Crohn's fissures represent a
p r i m a r y manifestation of the disease. T h e y are
usually associated w i t h shiny s k i n tags typical
of anal Crohn's disease, and the fissures m a y
lie laterally instead of cise to the m i d l i n e of
the anus.
T h e patient w i t h an anal fissure usually c o m plains of pain (frequently described as " t e a r i n g " )
occurring at the time of defecation. A b u r n i n g
pain may persist for several hours after a b o w e l
movement. Bright red bleeding m a y accompany
a b o w e l m o v e m e n t , b u t bleeding is usually m i n i m a l . A slight discharge may be present, and
occasionally, the discharge m a y cause itching.
A suspicion of fissure is easily confrmed b y
physical examination. Gentle separation of the
buttocks reveis the lower edge of the fissure at
the anal verge, where a sentinel tag may also be
seen. A deep gluteal cleft or tight spasm of the
sphincter may sometimes obscure the fissure.
CLINICAL SYMPOSIA

Pate 6

Incarcerated Hemorrhoids

Entire ring of internal


hiemorrtioids incarcerated
outside of anal canal

Injection of
local anesttietic
with epinephrine
and hyaluronidase

Manual compression
results in dissipation
of edema

Reduced hemorrhoids
then treated by
standard techniques
(internal sphincterotomy
if spasm present)

JOMNA.CRAiq-/AD
CIBA

Prolapsed tissue
reduced
Band ligation
of infernal
hemorrhoids

Excisin of
external hemorrhoids

VOLUME 37,

NUMBER 6

11

Pate 7

Anal F i s s u r e
Edematous
skin tag

Hypertrophied
anal papilla

Fissure
with exposed
internal
, ^ C ^ ^ ^ sphincter
* in base
'^

Edematous
skin tag
Classic anal fissure composed
of fissure, sentinel edematous
skin tag, and hypertrophied
anal papilla

Sentinel skin tag (shows fissure


on inspection) may be confused
with hemorrhoid
External
sphincter

Fissure predilection
for midline locus
may be related to
poor support by
external sphincter
in these reas

jaHNA.CRAiq-/AD
CIBA

Sentinel
skin tag

Infernal
sphincter
Hypertrophied
anal papilla

Fissures may be superficial


or deep chronic ulcers, which
expose infernal sphincter

12

CLINICAL SYMPOSIA

D i g i t a l p a l p a t i o n and anoscopic examination


m a y be impossible because of the severe p a i n
associated w i t h an acute fissure. It is imperative,
however, that these examinations be p e r f o r m e d
at a later time to exelude other rectal lesions.
A careful h i s t o r y must be taken to exelude
Crohn's disease. If the fissure is located laterally
instead of cise to the m i d l i n e , testing for systemic disease (leukemia, tuberculosis, syphilis,
or Crohn's disease) must be done first. If a fissure does not heal after adequate treatment,
biopsy is necessary to rule out carcinoma.
Treatment. T h e course of treatment depends
u p o n the severity of the pain a n d the c h r o n i c i t y
of the disease. M o s t fissures heal spontaneously
Topical treatment of the perianal s k i n w i t h o i n t ments is of little valu. The use of suppositories
is also contraindicated since they are p a i n f u l to
insert a n d come to rest above the fissure. Careful
c o n t r o l of diet to avoid constipation is more
i m p o r t a n t . The passage of a soft, b u l k y stool can
prevent f u r t h e r i n j u r y to the anus, and p h y s i o logic anal dilatation m a y also be advantageous.
W a r m soaks help to relieve sphincter spasm.
T h e great m a j o r i t y of fissures heal w i t h this k i n d
of conservative treatment. Contractile a b n o r m a l ities of the internal sphincter are often associated
w i t h anal fissures; these abnormalities usually
disappear after the fissure heals. However, deep,
chronic fissures associated w i t h a sentinel tag
and, occasionally, a h y p e r t r o p h i e d anal papilla
require more aggressive management.
Early i n this century, excisin was the recomm e n d e d surgical treatment for fissures. Excising
the fissure usually resulted i n healing, b u t sometimes the attendant " k e y h o l e d e f o r m i t y " of the
anus resulted i n fecal seepage. Since the floor of
the fissure is composed of exposed fibers of the
internal sphincter, excising a fissure was actually
t a n t a m o u n t to d i v i d i n g a p o r t i o n of the i n t e r n a l
sphincter (sphincterotomy). Excellent results can
be achieved if the internal sphincter is d i v i d e d
laterally rather t h a n at the m i d l i n e (Pate 8). A
lateral s p h i n c t e r o t o m y does not crate a postoperative keyhole d e f o r m i t y
S p h i n c t e r o t o m y may be p e r f o r m e d u n d e r
local anesthesia. Both an " o p e n " m e t h o d ( i n c i sin of the o v e r l y i n g a n o d e r m and direct exposure of the sphincter) and a " c l o s e d " m e t h o d
(divisin of the sphincter subcutaneously) have
been successful. A n a l dilatation, occasionally
r e c o m m e n d e d , forcefuUy disrupts the fibers of
the i n t e r n a l sphincters; general anesthesia is
often necessary for this procedure.
S p h i n c t e r o t o m y s h o u l d be reserved o n l y for
chronic fissures that have not healed despite
VOLUME 37,

NUMBER 6

adequate conservative therapy A p p r o x i m a t e l y


98% of all fissures heal foUowing sphinctero t o m y H o w e v e r , there is a small incidence of
partial anal incontinence foUowing sphincteroto m y , so careful patient selection is m a n d a t o r y
Because of an increased incidence of i n c o n t i nence of flatus, elderly patients w i t h decreased
anorectal sensation are generally not ideal c a n d i dates for i n t e r n a l s p h i n c t e r o t o m y
Anorectal Abscess and Fstula in A n o
Probably 95% of all anorectal suppurative
disease arise f r o m infections of the anal glands
(cryptogenic origin). Acute i n f e c t i o n of an anal
gland leads to an anorectal abscess, w h i l e the
chronic stage of infection appears as a fstula
in ano (Pate 9).
The muscular a n a t o m y of the anorectal regin
consists of a tube w i t h i n a tube. The inner tube
(the i n t e r n a l sphincter) is the h y p e r t r o p h i e d
c o n t i n u a t i o n of the circular s m o o t h muscle of
the large b o w e l . The outer tube is composed of
the puborectalis muscle a n d the external anal
sphincter The anal glands lie i n the space (the
intersphincteric plae) between these c y l i n d r i c
muscles, and they e m p t y into anal crypts at the
level of the dentate line t h r o u g h ducts that traverse the internal sphincter
C l i n i c a l features and diagnosis. Infection of
an anal gland leads to the f o r m a t i o n of a local
abscess i n the intersphincteric plae. The clinical
presentation, natural history, and proper treatm e n t of anorectal abscess a n d fstula i n ano are
easily u n d e r s t o o d if it is recognized that the d i s ease originates as an intersphincteric abscess.
As the abscess enlarges, it escapes the confnes
of the intersphincteric plae and spreads i n one
of several possible directions to f o r m a perianal
abscess or ischiorectal abscess. A perianal abscess,
the most c o m m o n of all anorectal abscesses,
results w h e n pus spreads d o w n w a r d , between
the t w o sphincters, to f o r m a tender, e r y t h e m a tous bulge at the anal verge. A n ischiorectal
abscess is f o r m e d w h e n a g r o w i n g intersphincteric abscess penetrates the skeletal muscle of
the external sphincter b e l o w the level of the
puborectalis and expands into the fat of the
ischiorectal fossa. These abscesses can become
quite large, because the levator ani (the u p p e r
border of the ischiorectal fossa) slopes u p w a r d .
T h u s , an ischiorectal abscess may be palpated
as a bulge above the puborectalis, a l t h o u g h it
actually lies below the levator ani musculature.
In contrast to the perianal abscess, this abscess
seldom presents as a visible bulge because of
the large potential space i n the ischiorectal fossa.
13

Lateral Internal Sphincterotomy


Closed technique

Fissure
Blade then moved
medially, dividing
inferior V3 to V2
of internal sphincter

Internal
sphincter
External
sphincter

Skin incisin
made external
to anal verge

Intersphincteric
plae

Infernal sphincter divided,


external sphincter, anoderm,
and longitudinal muscle
remain intact

Blade insertad in
intersphincteric groove
and passed cephalad in
intersphincteric plae to
leve! of dentate line

Open technique

Intact
anoderm

External
sphincter
Hypertrophied band
of internal sphincter
freed and elevated
into incisin

Infernal sphincter divided;


wound usually left open
for drainage
JOHNA.CRAIC^AD
CIBA

14

I
CLINICAL SYMPOSIA

Anorectal A b s c e s s and Fstula in Ano


Cryptoglandular Origin Theory

Inflammation
of anal crypts
(origin)

Acute abscess formation


in intersphiincteric plae
(acute pilase)

Formation of
fstula in ano
(chronic phase)

E x t e n s i n of i n t e r s p h i n c t e r i c a b s c e s s

JOHNA.CRAiq^AD
GIBA

Acute
abscess

Chronic
fstula

Supralevator
abscess
Extrasphincteric
fstula
Puborectalis
muscle
Intersphincteric
abscess (origin)
Ischiorectal
abscess
Transsphincteric
fstula

Intersphincteric
fstula

Perianal
abscess

Upward extensin of acute inflammation


results in supralevator abscess, lateral
in ischiorectal abscess; and downward
in perianal abscess
VOLUME 37,

NUMBER 6

Chronic inflammation results in


communication of abscess sites
with surface, causing fstulas

15

As a result, the abscess p r e f e r e n t i a l l y expands


u p w a r d rather t h a n p r o t r u d i n g t h r o u g h the
s k i n of the b u t t o c k . Rarely, an i n t e r s p h i n c teric abscess may e x p a n d u p w a r d between the
circular i n t e r n a l sphincter and the external
sphincter, f o r m i n g a supralevator abscess.
Treatment. Perirectal abscesses s h o u l d be
drained i m m e d i a t e l y w i t h o u t w a i t i n g for fluctuance or erythema to develop. A n t i b i o t i c s are n o t
indicated a n d s h o u l d be used o n l y i n the presence of specific disordersextensive cellulitis,
diabetes, or other states of c o m p r o m i s e d i m m u n i t y If the diagnosis is i n d o u b t , e x a m i n a t i o n
u n d e r regional anesthesia s h o u l d be p e r f o r m e d .
W i t h adequate anesthesia, the abscess can be
detected and localized b y digital e x a m i n a t i o n .
A n intersphincteric abscess is treated d e f i n i tively b y excising the infected c r y p t and perf o r m i n g an internal sphincterotomy, w h i c h u n r o o f s
and drains the abscess. H o w e v e r , if the i n f e c t i o n
has developed i n t o a perianal or an ischiorectal
abscess, adequate drainage of the abscess cavity
must first be done by inserting a small m u s h r o o m catheter t h r o u g h a stab w o u n d made i n the
s k i n o v e r l y i n g the abscess (Pate 10). Drainage
alone results i n complete r e s o l u t i o n of the infection i n about 50% of the patients. U n f o r t u n a t e l y ,
i n the other 50% of patients, a fstula i n ano
f o r m s . T h i s fstula results i n a localized chronic
i n f e c t i o n that is characterized b y i n t e r m i t t e n t
tenderness and drainage. The fstula consists of a
chronically infected tract w i t h an internal o p e n ing located i n a c r y p t at the level of the dentate
line and an external o p e n i n g located at the d r a i n age site of the earlier abscess. It is important to
drain the abscess as cise as possible to the anus to
avoid a lotig jistula tract.
T h e a p p r o p r i a t e treatment for fstula i n ano
is, of course, dependent u p o n the a n a t o m y a n d
location of the fstula tract. Goodsall's rule states
that if the anus is bisected b y a line i n the f r o n t a l
plae, an external o p e n i n g anterior to the line
w i l l connect to an i n t e r n a l o p e n i n g b y a short,
direct fstula tract. H o w e v e r , if the external
o p e n i n g is located posterior to this i m a g i n a r y
line, the fstula tract f o l l o w s a c u r v e d course to
an i n t e r n a l o p e n i n g i n the posterior m i d l i n e .
T h i s rule, w h i l e useful, is not i n f a l l i b l e . Occasionally, an external o p e n i n g anterior to the
i m a g i n a r y bisecting line connects to an i n t e r n a l
o p e n i n g i n the posterior m i d l i n e . Because of its
shape, this fstula is usually called a "horseshoe
fstula."
Horseshoe fstulas usually have an i n t e r n a l
o p e n i n g i n the posterior m i d l i n e of the anus
and m a y extend a n t e r i o r l y and laterally to b o t h
16

ischiorectal spaces b y w a y of the deep space.


The anterior extensions of the horseshoe tracts
can t h e n be d r a i n e d b y a secondary o p e n i n g ,
a v o i d i n g a long s k i n incisin that w o u l d u n r o o f
the entire tract (Pate 11).
If a perianal abscess develops i n t o a fstula
in ano after p r i m a r y drainage, the resultant
intersphincteric fstula is best treated b y an
internal s p h i n c t e r o t o m y that u n r o o f s the tract
and accompanies excisin of the c r y p t .
A fstula i n ano that f o l l o w s drainage of an
ischiorectal fossa abscess is usually a transsphincteric fstula, since the tract crosses the
lower p o r t i o n of the external sphincter T h e fst u l o t o m y r e q u i r e d to u n r o o f this tract results
in an internal s p h i n c t e r o t o m y as w e l l as d i v i sin of a p o r t i o n of the external sphincter
(Pate 12). If the tract lies b e l o w the puborectalis,
the external sphincter can usually be d i v i d e d at
the site of the fstula tract w i t h o u t loss of c o n tinence. T h e puborectalis m u s t not be d i v i d e d ,
or incontinence w i l l i n v a r i a b l y ensue.
Differential diagnoses. A l t h o u g h most anorectal s u p p u r a t i v e diseases begin as i n t e r s p h i n c teric infections, other disease entities must be
considered if the p a t h o l o g y appears atypical.
A careful h i s t o r y and physical e x a m i n a t i o n is
m a n d a t o r y to exelude Crohn s disease, a d i s ease f r e q u e n t l y complicated b y complex p e r i anal abscesses a n d fstulas. Special expertise
is r e q u i r e d to treat anal suppurative disease
associated w i t h C r o h n ' s disease.
Tuberculosis is n o w an u n u s u a l cause for anal
s u p p u r a t i v e disease. P u l m o n a r y tuberculosis is
n o w almost always detected b y chest x-ray Actinomycosis s h o u l d be suspected if t y p i c a l " s u l p h u r
g r a n u l e s " are seen associated w i t h a perianal
i n f e c t i o n . Pilonidal disease can sometimes be
confused w i t h a posterior perirectal abscess, b u t
careful e x a m i n a t i o n reveis that there is no
c o m m u n i c a t i o n w i t h the anus. H a i r may be
obtained f r o m the abscess cavity w h e n the p i l o n i d a l abscess is d r a i n e d , i n d i c a t i n g the true
nature of the disease. Hidradenitis
suppurativa
may also m i m i c cryptogenic s u p p u r a t i v e disease,
b u t closer e x a m i n a t i o n reveis that the disease
does n o t extend i n t o the anal canal.
Perianal Hidradenitis

Suppurativa

C l i n i c a l features. H i d r a d e n i t i s is an i n f e c t i o n
of the cutaneous apocrine glands. It is m o r e
c o m m o n i n blacks t h a n i n other races. T h e frst
clinical m a n i f e s t a t i o n of i n f e c t i o n i n v o l v i n g
these large, c o m p o u n d t u b u l a r secretory glands
is a tender, localized n o d u l a r i n d u r a t i o n i n
the perianal rea. T h e infected glands t e n d
CLINICAL SYMPOSIA

to rupture and f o r m subcutaneous sinus tracts.


Pressure over the infected rea may cause pus
to exude f r o m one or more shallow sinus tracts.
The infection may spread by direct extensin,
and the perianal skin can become a honeycomb
of superficial abscesses and sinuses. The infection can extend into the perineum, labia, and
scrotum. The axilla can be involved w i t h a s i m i lar process. This condition may occasionally
m i m i c a complicated anal fstula, but the infection stops at the anal verge, since there are no
apocrine glands i n the anal canal.
Treatment. A n t i b i o t i c s have no valu i n the
treatment of hidradenitis. Acute abscesses must
first be drained for relief of pain, but the only
effective treatment is complete excisin of all
infected s k i n . Small reas heal by contracture;
large reas, however, may require split-thickness
or pedicle grafts after excisin. Recurrence is
frequent, and any recurrent infections must be
excised immediately
Rectovaginal Fistula
A rectovaginal fistula is a communication
between the epithelial-lined surfaces of the rect u m and vagina. This definition exeludes the
more c o m m o n anal vaginal fistula, a c o m m u n i cation between the anal canal distal to the d e n tate line and the vagina.
These fstulas may be classified according to
their location. The rectal opening i n a low rectovaginal fistula is cise to the dentate line w i t h the
vaginal opening just inside the vaginal fourchette.
In a high rectovaginal fistula, the vaginal opening
is near the cervix, and a midrectovaginal fistula
resides between these t w o limitations. The size
of rectovaginal fstulas can vary f r o m defects less
than 1 m m i n diameter to defects i n v o l v i n g the
entire posterior vaginal wall.
Etiology There are a n u m b e r of causes for
rectovaginal fstulas, and the etiology varies w i t h
the location of the fistula. C o m m o n causes of
low rectovaginal fstulas are third-degree obstetric tears i n w h i c h the repair has been unsuccessful, m i d l i n e episiotomy repairs, w h i c h have
become infected or in w h i c h a suture has penetrated the rectum, penetration of the rectum by
a fishbone or other similar foreign b o d y ; and
Crohn's disease.
Midrectovaginal fstulas may result f r o m
extensin of an undrained ischiorectal abscess,
Crohn's disease, surgical excisin or f u l g u r a t i o n
of an anterior rectal t u m o r , c h i l d b i r t h trauma,
or radiation i n j u r y (especially foUowing pelvic irradiation for carcinoma of the cervix or
endometrium).
VOLUME 37,

NUMBER 6

H i g h rectovaginal fstulas can also be caused


by Crohn's disease, radiation injury, operative
i n j u r y (especially d u r i n g hysterectomy), and
diverticulitis. M o s t vaginal fstulas caused by
diverticulitis are actually sigmoidovaginal fstulas. Carcinoma of the rectum, cervix, or vagina
may also result i n a rectovaginal fistula at any
level, but these cases are rare.
Treatment. The treatment of a rectovaginal
fistula obviously depends u p o n its etiology, the
l i k e l i h o o d of spontaneous healing, and the
severity of symptoms. Fstulas caused by foreign
bodies frequently heal foUowing removal of the
foreign body If the fistula is caused by an infect i o n , appropriate treatment of the infection
usually results in healing. A significant n u m b e r
of rectovaginal fstulas caused by obstetric
trauma heal spontaneously, so it is wise to wait
at least 6 months before attempting to surgically
repair these injuries. This waiting period allows
i n f l a m m a t i o n to subside, facilitating repair if
healing does not occur Fstulas caused by
Crohn's disease, radiation injury, or cncer
almost never heal spontaneously
There are numerous ways to repair rectovaginal fstulas; since a complete review of all these
methods is beyond the scope of this monograph,
only a few of the b e s t - k n o w n approaches are
mentioned here.
H i g h rectovaginal fstulas can often be treated
o n l y w i t h a transabdominal approach, while
low or midrectovaginal fstulas, especially those
caused by obstetric trauma, can frequently be
repaired transanally Bowel preparation consists
of a mechanical cleansing rgimen, and a n t i b i o t ics are administered in a manner identical to that
used for colectomy The operation is performed
using a spinal anesthetic, w i t h the patient i n the
prone jackknife position. A protecting colost o m y is not necessary
Exposure is gained using an operating anoscope. A n anorectal advancement flap consisting
of mucosa, submucosa, and circular muscle is
created, ncluding the rectal opening of the fstula in the flap. The cephalad base of the flap
should be twice the size of the caudal apex, to
assure adequate blood supply The flap is
advanced over the vaginal defect, and the apex of
the flap containing the fstulous defect is excised
(Pate 13). The attenuated perineal body is
reconstructed w i t h absorbable sutures. The flap
is sutured in place, restoring n o r m a l anatomy
If a sphincteric i n j u r y is also present, as is
often the case i n obstetric injuries, the sphincters
are repaired using the technique described in the
section discussing incontinence (page 22).
17

Pate 10

Surgical Management of Anorectal A b s c e s s

Points of incisin
excised; wound
left open to drain

Ischiiorectal abscess may be


palpated above anorectal ring,
althiough located inferiorly
18

Wound left open


for drainage

Abscess incised and


loculations broken down

IVIusfiroom catheter inserted


to insure drainage
CLINICAL SYMPOSIA

Pate 11
Surgical Management of H o r s e s h o e Fistula
Internal
opening
Fistula
tract
External
opening

Prob

Main posterior tract


identified with prob
Horseshoe fistula with
external openings
anterior to midanal
line and internal
opening in posterior
midline

JOHNA.CRAie^;^D
GIBA

Short posterior
portion of tract
unroofed and
involved crypt
excised

JQHNA.CRA!q-/AD
GIBA

Anterior extensions
curetted and drained
via Penrose drains
through secondary
incisions along tracts,
avoiding long incisin

VOLUME 37,

NUMBER 6

19

Fstulas resulting f r o m Crohn's disease can


rarely be corrected by localized surgical procedures. Because of persistent feculant vaginal
discharge, a b d o m i n a l perineal proctocolectomy
is usually the procedure of cholee for these fstulas. However, high enterovaginal fstulas resulting f r o m Crohn's disease of the sigmoid colon or
the terminal i l e u m can be closed by resecting the
diseased segment of intestine.
Rectovaginal fstulas due to pelvic irradiation
are seldom amenable to transanal repair Recurrent cncer as the cause of the fstula must be
excluded, biopsies of the fstula tract may be
necessary to do this. Bricker has described an
onlay patch procedure that has been successful
in selected patients w i t h rectovaginal fstulas
caused by irradiation.
A n a l Incontinence
The inability to prevent the passage of flatus
or feces is referred to as anal incontinence. The
degree of incontinence varies f r o m an occasional
episode of involuntary passage of flatus to the
complete inability to prevent passage of solid
feces. Two i m p o r t a n t factors i n the maintenance
of continence are the consistency of the stool and
the efficiency of the anal sphincters. A n o r m a l
sphincter may be incapable of preventing the
passage of l i q u i d feces, while a weak sphincter
mechanism may satisfactorily control the passage of solid feces.
Etiology I n f l a m m a t o r y b o w e l disease, irritable bowel syndrome, infections gastroenteritis,
and, rarely, mucus-secreting colorectal tumors
allow the entrance of large volumes of l i q u i d
stool into the rectal ampulla, o v e r w h e l m i n g the
n o r m a l physiologic capacity of the sphincter
A l t e r a t i o n i n the patient's ability to discrimnate between flatus, l i q u i d feces, or solid feces
may occur w i t h nondistensible rectum, resulting
f r o m chronic ulcerative proctitis. Patients w i t h
low anterior proctosigmoidectomy w i t h colorectal anastomosis often experience difficulty i n
discriminating rectal contents d u r i n g the frst
few m o n t h s foUowing the operation. This c o n d i tion usually improves w i t h time.
The motor innervation of the levator ani and
external anal sphincter is supplied by the p u d e n dal nerves (S2, 53, 54). Direct i n j u r y to the
pudendal nerve may result i n anal incontinence.
It has been suggested that the incontinence often
seen i n patients w i t h rectal prolapse may be due
to stretch i n j u r y of the m o t o r nerves that innervate the anal sphincters. Lesions of the cauda
equina result i n a flaccid paralysis of the sphincters; spinal cord lesions cause a spastic paralysis.
20

I m p a i r m e n t of the anorectal musculature is a


very i m p o r t a n t cause of incontinence. Impairm e n t of the anal sphincter mechanism can be
neurologic or muscular Neurologic causes of
incontinence may be f u r t h e r subdivided into
sensory i m p a i r m e n t or motor i m p a i r m e n t . Scleroderma or dermatomyositis and other muscular
diseases may affect the anal sphincter resulting
in impaired continence. A mechanical impairment of the n o r m a l a p p r o x i m a t i o n of the walls
of the anal canal can result i n varying degrees
of incontinence; prolapsing hemorrhoids or anal
tumors can prevent closure of the anal canal.
Direct i n j u r y to the anal sphincters is a fairly
c o m m o n cause of anal incontinence. The internal sphincter is a major component i n the m a i n tenance of the n o r m a l resting tone of the anal
canal. Divisin of the internal sphincter, an
operation frequently done to treat a chronic anal
fssure, may result i n partial incontinence w i t h
i n v o l u n t a r y passage of flatus, especially i n
patients w i t h irritable b o w e l syndrome.
Divisin of the external anal sphincter can
occur d u r i n g the surgical treatment of c o m p l i cated anal fstulas, or as a result of m i d l i n e episio t o m y p e r f o r m e d to faciltate vaginal delivery If
the sphincters are reapproximated d u r i n g repair
of the episiotomy, satisfactory continence usually is maintained. However, w o u n d infection
may result i n the b r e a k d o w n of the sphincter
repair w i t h ensuing incontinence.
Clinical features and diagnosis. The clinical
evaluation and treatment of the patient w i t h
anorectal incontinence is determined b y the
extent to w h i c h the p r o b l e m interferes w i t h lifestyle and social activities.
A detailed history is essential, and usually the
cause of the incontinence is determined by history alone. A thorough anorectal examination is
mandatory Fecal soilage of the undergarments
or a perineal pad can identify the severity of the
p r o b l e m . Scarring of the anal canal may reveal
the site of sphincter laceration, or a patulous anal
canal may suggest i m p a i r m e n t of the nerve
supply The patient should be asked to strain or
cough d u r i n g the examination i n an effort to
reveal perineal descent or mucosal prolapse.
D i g i t a l rectal examination allows evaluation of
sphincter tone, and a d i s r u p t i o n of the anal
sphincter may be palpable. Sigmoidoscopic
examination rules out anorectal tumors. Careful
inspection of the rectal mucosa should be conducted to exelude a solitary rectal ulcer that may
be associated w i t h rectal prolapse. If the cause of
the incontinence is not obvious, manometric
studies may be h e l p f u l .
CLINICAL SYMPOSIA

Pate 12

Surgical Management of Fistula in Ano

/
Puborectalis
muscle

Midanal
line

Intersphincteric
fistula
G o o d s a l l ' s rule

Fstulas with external openings anterior


to midanal line usually connected to
internal opening by short, straight tract.
Posterior external openings follow curved
course to internal opening in posterior
midline

Transsphincteric
fistula

Surgical management of intersphincteric and low


(below puborectalis) transsphincteric fstulas
involves unroofing tract. Only internal sphincterotomy in first case- internal sphincterotomy involving
portion of external sphincter in latter case. Divisin
of puborectalis muscle results in incontinence,
so high fstulas not treated by sphincterotomy

Fistulotomy technique

VOLUME 37,

NUMBER 6

21

Anorectal m a n o m e t r y can determine the resting basal pressure and mximum squeeze pressure of the sphincters. These measurements and
the patient's ability to retain saline infused into
the rectum can aid i n the diagnosis and management of incontinence due to the irritable b o w e l
syndrome. M a n o m e t r i c studies are also very
useful i n the evaluation of diseases directly
affecting muscle cells, such as scleroderma or
dermatomyositis.
Treatment. The management of incontinence
depends o n the cause of the disorder and the
severity of symptoms. Patients w i t h m i n o r
degrees of incontinence may benefit f r o m b u l k
additives like p s y l l i u m seed preparations to
ensure a soft and f o r m e d stool. The use of glycerin suppositories allows the rectal ampulla to
be evacuated on a routine schedule. Biofeedback mechanisms, utilizing anorectal m a n o m etry, have been successful i n controlling m i n o r
incontinence caused b y surgical i n j u r y to the
sphincters.
Incontinence, caused b y a laceration of the
anal sphincters and unresponsive to conservative
measures, can be corrected b y surgical reconstruction of the divided muscle (Pate 14). The
d i v i d e d ends of the sphincter are dissected f r o m
the s u r r o u n d i n g soft tissue. Fibrous scar tissue
should not be removed; this tissue should be
used i n a "pants-over-vest" technique of muscle
reconstruction. The fibrous scar tissue w i l l h o l d
sutures readily, i n contrast to muscular tissue.
A protecting colostomy is seldom necessary,
and results f r o m this repair have been quite
satisfactory
Silver wire or other prosthetic material placed
subcutaneously a r o u n d the anus has been used
to m a i n t a i n the reduction of rectal prolapse and
to i m p r o v e anal continence. U n f o r t u n a t e l y , the
circumanal wire technique is often associated
w i t h infection and fecal impaction.
Patients w i t h intensive sphincteric injuries
(impalement injuries or gunshot w o u n d s ) have
been reported to benefit f r o m a gracilis muscle
sling. The gracilis muscle f r o m the thigh is used
to encircle the anus to maintain continence; the
sling s h o u l d be reserved for patients w i t h
sphincteric damage not suitable for direct repair
Finally, if the cause of incontinence is such
that surgical repair of the sphincters cannot
be successfully p e r f o r m e d , a colostomy may
be created to achieve satisfactory control of
e l i m i n a t i o n . However, the previously m e n tioned methods of controlling incontinence are
generally sufficient, and a colostomy is rarely
required.
22

Rectal Prolapse
Rectal prolapse, or procidentia, is the c i r c u m ferential descent of the rectum through the anal
sphincters (Pate 15). This condition is most
c o m m o n at the extremes of Ufe (in children
under 2 years and i n the elderly). W o m e n are
more susceptible than men, but m u l t i p a r i t y does
not seem to be an etiologic factor
In children, the prolapse most often consists
of mucosa only and is therefore called a partial
prolapse. However, w h e n the entire thickness of
the rectal wall protrudes b e y o n d the anus, the
condition is called a complete prolapse.
Etiology There are several theories as to the
cause of rectal prolapse, and one theory does not
necessarily rule out the others. It has been suggested that (1) a rectal prolapse mimics a sliding
hernia, as evidenced b y the a b n o r m a l l y deep
cul-de-sac (or pouch) of Douglas; (2) a weakened
pelvic musculature and lax anal sphincters allow
the rectum to protrude; or (3) the prolapse precedes the sphincteric weakness; the ensuing
incontinence frequently associated w i t h p r o c i dentia is caused b y nerve entrapment or the
resulting nerve stretching.
Clinical features and diagnosis. In patients
w i t h procidentia, the rectum loses the n o r m a l
fixation i n the h o l l o w of the sacrum and lies
anterior to the sacral concavity Thus, the lower
intestine becomes a straight tube, and increased
intraabdominal pressure produces an intussusception that causes rectal mucosa to p r o t r u d e
through the anus.
The partial prolapse usually seen i n chUdren is
a s e l f - l i m i t i n g condition. The p r o b l e m d i m i n ishes w i t h age, perhaps as a result of the development of the sacral concavity Both partial and
complete prolapse can occur i n the adult. H o w ever, i n partial prolapse, the p r o t r u d i n g mucosa
seldom extends farther than 4 cm beyond the
anal verge; in true (complete) prolapse, this distance is usually greater Complete rectal prolapse
involves protrusion of the entire bowel w a l l ,
therefore, the thickness of the p r o t r u d i n g w a l l is
greater than w h e n o n l y mucosa is p r o t r u d i n g . I n
complete prolapse, the mucosal folds are concentric; i n partial prolapse, the mucosal folds are
radial. N o r m a l tone of the anal sphincters suggests partial prolapse; laxity of tone usually i n d i cates complete prolapse.
Treatment. Partial prolapse i n children can
usually be treated b y manually replacing the
p r o t r u d i n g tissues above the anus; it may be
necessary to maintain the reduction b y strapping
the buttocks together Ensuring proper b o w e l
habits and avoiding constipation are i m p o r t a n t
CLINICAL SYMPOSIA

Pate 13
Rectovaginal Fistula Repair

Perineal body reconstructed


by plication over fistula
VOLUME 37,

NUMBER 6

Flap sutured in position


with interrupted sutures
23

preventive measures. Rarely, patients w i t h persistent s y m p t o m s may require treatment w i t h


submucosal injections of sclerosing agents.
The treatment of partial prolapse i n the adult
is similar to the treatment of third-degree
h e m o r r h o i d s t h e r e d u n d a n t mucosa is e l i m i nated b y ligation w i t h elastic bands. Excisin of
r e d u n d a n t mucosa and cryodestruction of p r o t r u d i n g mucosa can also correct partial prolapse.
N u m e r o u s surgical procedures have been
devised to treat complete prolapse of the rectum,
and considerable controversy persists as to treatment of cholee. The most successful approaches
involve resection of the r e d u n d a n t intussuscept i n g rectosigmoid colon and a procedure to reestablish n o r m a l pelvic anatomy by affixing the
rectum to the h o l l o w of the sacrum. I n order to
benefit f r o m any of these procedures, the patient
must be able to undergo laparotomy
O n e f r e q u e n t l y used procedure is a modificat i o n of the technique first described b y Ripstein.
This technique uses an encircling sling of m o n o filament mesh to secure the rectum to the sacr u m (Pate 16). The sling must be lose enough
so that fecal impaction does not occur postoperatively T h i s operation successfully controls the
prolapsing intestine. However, anal incontinence
associated w i t h procidentia often persists or
increases foUowing surgical correction of the
prolapse. Sometimes, this residual anal i n c o n t i nence improves w i t h time, so it is advisable to
wait at least 1 year (after prolapse surgery)
before t r y i n g to correct the incontinence surgically Electrical s t i m u l a t i o n of the anal sphincters
may also be useful i n patients w i t h residual
incontinence. Parks surgically repaired the levator ani t h r o u g h an intersphincteric approach. A
n u m b e r of patients successfully treated by this
m e t h o d have been cited i n the literature.
Fecal Impaction
Incomplete stool evacuation f r o m the rectal
a m p u l l a leads to accumulation of feces that
barden as fecal fluids are excreted or absorbed.
T h e mass of feces becomes so large and h a r d
that it cannot be passed t h r o u g h the anal canal.
Etiology The most c o m m o n causes of fecal
i m p a c t i o n are postoperative constipation, p r o longed bed rest, residual b a r i u m f r o m b a r i u m
enemas, and overuse of constipating drugs, for
example, codeine or meperidine.
The large bolus of feces i n the rectum causes
reflex i n h i b i t i o n of the external sphincter L i q uids and soft stool then pass a r o u n d the fecal
bolus and, paradoxically, diarrhea and i n c o n tinence occur A digital examination can easily
24

c o n f i r m the diagnosis, revealing a large, h a r d


mass of stool i n the rectal a m p u l l a .
Treatment. The best course of treatment is
prevention. The left colon should be evacuated,
using enemas, p r i o r to any a b d o m i n a l or anorectal operation. P s y l l i u m seed preparations or
m i l d laxatives should be used i n the postoperative p e r i o d . Laxatives should be considered
foUowing G I radiography to assure complete
evacuation of b a r i u m . M i l d laxatives or enemas
should be prescribed for b e d r i d d e n patients to
assure regular b o w e l evacuation.
Once fecal i m p a c t i o n has occurred, evacuation
should be achieved b y the least traumatic
m e t h o d . If the patient is not in distress, oral laxatives should be tried first. Enemas, usually tap
water enemas, may also provide relief. D i o c t y l
s o d i u m sulfosuccinate and vegetable o i l enemas
are very h e l p f u l i n difficult cases.
If the fecal bolus cannot be softened and evacuated b y laxatives and enemas, digital m a n i p u l a tion is necessary to remove the lower p o r t i o n of
it. It is not necessary to remove the entire fecal
bolus digitally; the goal should be to remove
only the lowest p o r t i o n and allow enemas to
soften the r e m a i n i n g stool.
A f t e r the i m p a c t i o n has been evacuated, preventive measures are of paramount importance.
A h i g h - b u l k diet and oral laxatives (if diet alone
is not sufficient) are mandatory The use of constipating drugs s h o u l d be avoided, if possible.
Pruritus A n i
Pruritus ani is a s y m p t o m complex, not a specific disease. A careful history and physical
examination should be a matter of course to rule
out any easily treatable cause.
Etiology and clinical features. P i n w o r m s
(Enterobius vermicularis) are the most c o m m o n
cause of perianal i t c h i n g i n c h i l d r e n , and the
parasites can be transmitted to other f a m i l y
members. The w o r m s come out of the anus at
night and deposit eggs on the perianal s k i n ,
causing intense n o c t u r n a l p r u r i t u s .
C o m m o n anal lesions (prolapsing hemorrhoids, villous t u m o r s of the rectum, and rectal
prolapse) often cause excessive moisture and
itching i n the perianal regin. The appearance of
the perianal s k i n varies w i d e l y f r o m patient to
patient. I n m i l d cases, the s k i n may appear
completely n o r m a l . If the c o n d i t i o n is acute, the
skin may be erythematous and weeping, w i t h
numerous excoriations. I n chronic cases, the s k i n
is thickened, leathery, and w h i t e .
W h i l e a complete history and physical examination w i l l i d e n t i f y any obvious causes of
CLINICAL SYMPOSIA

Pate 14

1 ^

Sphincter Repair Technique


Incisin site
exposes scarred
sphincter

Skin and
mucosal
flap

Functional
sphincter
Scarred
nonfunctional
sphincter

Flap of skin and rectal


mucosa elevated to
expose sphincter
Sphincter dissected free
and divided. Fibrous scar
should be preserved
JOHNA.CRAiq^AD
GIBA

Flap repaired
and incisin
closed

Sphincter overlapped
and fibrotic end of each
sutured to opposing body
VOLUME 37,

NUMBER 6

25

pr.uritus i n over 90% of patients, the etiology is


obscure. Before seeking professional help, many
patients seek relief by a p p l y i n g numerous t o p i cal ointments and medications, a practice that
frequently exacerbates the c o n d i t i o n and makes
its cure more difficult. In the majority of patients,
pruritus ani is caused b y one or b o t h of the f o l l o w i n g factorslocal hygienic practices and
c o n s u m p t i o n of certain foods.
Pruritus ani attributed to local hygiene p r o b lems can be divided into t w o categories: inadequate or careless cleansing of the perianal skin,
w h i c h allows fecal matter to irrtate the skin, and
overzealous cleansing of the anus and perianal
skin. The latter category is by far the most
c o m m o n of the t w o . Symptoms due to inadequate perianal cleansing can only be remedied
by the patient; appropriate cleansing foUowing
defecation is the only cure. Overzealous cleansing is more difficult to recognize. To alleviate the
itching, patients overzealously clean the perianal
rea w i t h frequent washings and a p p l y topical
ointments that keep the regin moist, causing
further irritation.
In p r o b a b l y o n e - t h i r d of patients w i t h pruritus
ani, a dietary history w i l l reveal the causative
agent. Coffee, tea, cola, beer, chocolate, and
tomatoes can all induce perianal itching. Excessive c o n s u m p t i o n of these products is very
c o m m o n among patients w i t h pruritus ani.
A b s t a i n i n g f r o m these foods for about 2 weeks
alleviates most of the s y m p t o m s .
Treatment. Pinworms are easily confirmed by
microscopic examination of an adhesive cellulose tape swabbed on the perianal skin, w h i c h
reveis Enterobius eggs. Treatment w i t h piperazine citrate is curative.
If internal hemorrhoids are prolapsing and
cause perianal moisture, ligation of the hemorrhoidal tissue is indicated.
Patient education on the appropriate hygiene
of the perianal rea is the most i m p o r t a n t aspect
of treatment. Patients must be taught that
repeated washings and applications of medications are the source of their symptoms. A p r o gram of gentle but effective perianal hygiene
should be initiated.
Cleansing w i t h tissue should be discouraged,
instead, cotton moistened w i t h w a r m water is as
effective and m u c h less traumatic. Topical ointments should not be used since they only serve
to excorate the skin. The perianal rea should
be kept as d r y as possible to alleviate further
itching. A t h i n sheet of cotton i n the undergarments can help to absorb excess moisture. A f t e r
a shower, the patient should gently d r y the
26

perianal skin by patting w i t h soft towel, never


by harsh r u b b i n g . Finally, and most i m p o r t a n t ,
scratching the perianal rea o n l y aggravates and
prolongs the c o n d i t i o n . U n t i l adequate w i l l power is mustered to refrain f r o m scratching the
irritated tissues, all curative attempts w i l l fail.
O f t e n it is difficult to ascertain whether the
pruritus is caused by a dietary product or b y
overzealous cleansing, and i n fact, both may
be c o n t r i b u t i n g factors. A practical approach is
to encourage gentle hygienic measures as w e l l
as abstinence f r o m the c o m m o n dietary causes.
If this approach is faithfuUy f o l l o w e d , over 90%
of patients w i t h pruritus ani w i l l notice significant relief f r o m their symptoms i n 2 weeks.
SEXUALLY TRANSMITTED
ANORECTAL DISEASE
D u r i n g recent years, there has been a p r o f o u n d change i n the types and prevalence of
sexually transmitted diseases of the anus and
rectum. Factors c o n t r i b u t i n g to this change
include effective oral contraception, decreasing
use of the c o n d o m , increasing male homosexual
activity, liberalization of sexual mores, and other
u n k n o w n epidemiologic factors. C h l a m y d i a l
infections (nongonococcal urethritis and n o n specific genital infection) are n o w more c o m m o n
than gonococcal or treponemal diseases. I n c u r able viral diseases such as herpes and the
acquired i m m u n e deficiency syndrome ( A I D S )
have attracted the attention of not o n l y the m e d i cal profession but also the general public.
A n a l sexual practices among male homosexuals make this p o p u l a t i o n particularly vulnerable
to these diseases. O f t e n , sexually transmitted
anorectal diseases m i m i c nonvenereal i n f l a m m a tory processes, and it is not unusual for one
patient to present w i t h concurrent venereal diseases of different types.
Condylomata

Acuminata

Etiology. The c o m m o n anal wart is caused


by a paplUoma virus. T h i s group of viruses has
been associated w i t h malignant tumors i n some
animis, and occasionally cases of concurrent
condylomas and squamous cell carcinomas of
the anus have been reported i n humans. The
incubation period is f r o m 1 to 6 months. These
viruses are autoinoculable, a characteristic that
accounts for the frequent failures i n treatment.
Condylomata acuminata occur i n the anorectal
and urogenital regions, most frequently i n male
homosexuals. A n a l intercourse is a causative
factor i n about 90% of all patients w i t h anorectal
warts. Homosexual m e n have a m u c h higher
CLINICAL SYMPOSIA

Pate 15

Rectal Prolapse

Folds in mucosal prolapse


usually radial in orientation

Normal anatomic position


of rectum in sacral hollow

Loss of normal rectal fixation in sacral


hollow allows lower bowel to form straight
tube, which allows rectum to intussuscept
and prolapse. Deep pouch of Douglas
present; condition may be aggravafed by
weak pelvic musculature and lax sphincters

jaHNA.CRAiq^AD
GIBA

Partial prolapse
mucosa only)
Childhood type

Complete prolapse
(full-thickness
bowel wal
Adult type

VOLUME 37,

NUMBER 6

Complete prolapse folds generally circular


27

incidence of anal warts than urogenital warts.


O t h e r venereal diseases frequently accompany
anal condylomata acuminata.
Clinical features and diagnosis. M o s t patients
w i t h perianal warts present after noticing the
visible fleshy perianal growths. Pruritus is a
frequent complaint, and anal discharge, bleeding, and pain are occasionally present.
The diagnosis is usually obvious because of
the characteristic appearance of the warts. A n o s copy and proctosigmoidoscopy should be perf o r m e d on all patients w i t h the disease. The
majority of patients w i t h perianal warts may also
have warts i n the anal canal. Since other sexually transmitted diseases frequently accompany
condylomata acuminata, cultures for bacterial
pathogens; stool specimens for ova and parasites; pharyngeal, urethral, and rectal cultures
for gonorrhea, and serologic tests for syphilis
should be considered.
Occasionally, condylomata acuminata can be
confused w i t h the lesions of secondary syphilis,
condylomata lata, w h i c h are usually smoother,
flatter, and lighter i n color These lesions can occur
simultaneously w i t h condylomata acuminata.
Treatment. There are numerous treatments for
condylomata acuminata, b u t topical application
of 25% p o d o p h y l l i n suspended i n tincture of
benzoin is the most c o m m o n . The warts are
carefully and accurately painted w i t h this cytotoxic medication, it is i m p o r t a n t not to touch
adjacent n o r m a l skin w i t h the medication. A f t e r
6 hours, the medication is washed off. Treatments are repeated at w e e k l y intervals u n t i l all
warts are eradicated. This treatment is satisfact o r y only if the warts are small and few i n n u m ber If a modrate n u m b e r of warts are present,
the medication almost always is transferred to
adjacent anal and perianal skin, causing discomfort and p r u r i t u s .
Dichloroacetic acid, a caustic topical agent,
can also be used to treat anal warts. Using a
small w o o d e n applicator, the acid is applied
directly to the wart. The caustic action i m m e d i ately turns the fleshy wart frosty white. Treatments are repeated at w e e k l y intervals u n t i l the
disease is eradicated.
Frequently, treatment w i t h topical agents is
inappropriate because of the large n u m b e r of
warts. Electrocoagulation or a combination of
excisin and electrocoagulation, under local
anesthesia, is the most effective treatment for
these patients. The surgeon uses the cautery to
destroy each small wart, carefully preserving the
adjacent s k i n and anoderm. A l l warts should be
destroyed to lower the incidence of recurrence.
28

Patients are examined at w e e k l y intervals, and


any new warts are treated w i t h topical d i c h l o roacetic acid. Rarely, condylomata acuminata
repeatedly recur i n large numbers despite
aggressive treatment. Patients w i t h refractory
warts have been successfully treated w i t h a vaccine prepared f r o m their o w n warts.
Rarely, patients have giant condylomata acuminata i n v o l v i n g the penis and perianal regin
that appear to be histologically benign b u t
clinically behave as locally aggressive, invasive
carcinomas. These tumors (Buschke-Lowenstein
tumors) do not respond to conservative therapy
Radical surgical extirpation offers the o n l y
hope for cure or palliation.
Chlamydial Infections
Etiology The most prevalent sexually transmitted infections i n America today are caused by
chlamydial organisms. Recently, the n o n l y m p h o granulomatous (nonLGV) chlamydial organisms
have been recognized as a c o m m o n cause of
nonspecific urethritis, e p i d i d y m i t i s , and pelvic
inflammatory disease. A t least half of the genital
infections previously designated as "nonspecific" or "nongonococcal" are caused by the
n o n L G V chlamydial organisms.
The n o n L G V chlamydia are oblgate intracellular parasites that can pentrate only columnar
or transitional e p i t h e l i u m . The l y m p h o g r a n u l o matous (LGV) chlamydial organisms can also
pentrate mononuclear cells, w h i c h may account
for the p r o m i n e n t l y m p h a d e n o p a t h y of LGV
Clinical features and diagnosis. Infection may
be entirely asymptomatic, or nonspecific s y m p toms ncluding anal pain, pruritus, p u r u l e n t
discharge, and bleeding may be present. The
more severe forms of infection, especially
severe proctitis, usually indcate the presence of
an LGV type of chlamydia.
Diagnosis of chlamydial infections requires a
high Index of suspicion. Rising a n t i b o d y titers
indcate the presence of these infections. C u l tures require laboratories w i t h viral and tissue
culture capabilities and are quite costly

Treatment. C h l a m y d i a l infections should be


treated as soon as the diagnosis is suspected. The
cholee treatment for n o n L G V chlamydial infections is tetracycline or, as an alternative, e r y t h r o m y c i n . L G V chlamydial infections should be
treated w i t h tetracycline and sulfamides for a
mnimum of 21 days.
Gonorrhea
Clinical features and diagnosis. Rectal Neisse,ia gonorrhea infections are c o m m o n i n the
CLINICAL SYMPOSIA

;
|
i

Pate 16

Surgical Management of Rectal Prolapse


.Incisin made in redundant rectal
mesentery anterior to sacrum

Strip of monofilament mesh sutured to


anterior intraperitoneal surface of rectum
and then passed around both rectum
and 2-cm sigmoidoscope via mesenteric
incisin. Then monofilament mesh stapled
in this configuration to form ring

Sutures
Mesh

StapI
line

Stapler

Wings of sling trimmed and then fixed to


sacral promontory with heavy nonabsorbable
sutures, restoring rectum to its proper
position in sacral curve

JOHN A.

Postoperative view showing normal rectal


position and position of sling
VOLUME 37,

NUMBER 6

GIBA

lime
ROCTOLOan

male homosexual p o p u l a t i o n and frequently


accompany other venereal disease. The s y m p toms are quite varied, ranging f r o m none at all to
intense rectal pain accompanied by a viscid, y e l low discharge. Severe cryptitis or distal proctitis
is often seen on anoscopic examination.
Diagnosis can be made b y swabbing the rectal
mucosa w i t h a cotton-tipped applicator and then
c u l t u r i n g or plating on T h a y e r - M a r t i n or Stuart
mdium. Untreated rectal gonorrhea can result
in infection of sexual partners, septic arthritis,
endocarditis, perihepatitis, and meningitis.
Treatment. To prevent complications, treatm e n t should begin as soon as the disease is suspected. Several drugs (for example, penicillin,
tetracycline, a m p i c i l l i n , and spectinomycin) are
used for the treatment of gonorrhea. If the c u l tures for gonorrhea are positive, they should be
repeated after treatment, since treatment may
fail as m u c h as o n e - t h i r d of the time. However,
if the cultures for gonorrhea are negative,
the symptomatic patient should be treated as
described for n o n L G V c h l a m y d i a l infection. A l l
patients w i t h rectal gonorrhea should have a
serologic test for syphilis 3 months after treatment to rule out undetected syphilis.
Syphilis
A b o u t 70% of all patients w i t h syphilis are
male homosexuals. A l t h o u g h earlier descriptions
of anal chancres indicated this to be a painless
ulcerated lesin, anal chancres are usually
extremely p a i n f u l . The p r i m a r y chancre occurs
at the anal verge or i n the anal canal and rarely
involves rectal mucosa. Isolated proctitis due to
syphilis can occur w i t h o u t a concomitant chancre. Inguinal adenopathy is c o m m o n .
Diagnosis. D a r k - f i e l d microscopy is not u s u ally available i n most laboratories, b u t serum
obtained f r o m the base of the ulcer (cleansed
w i t h acetone) can be dried and stained w i t h
fluorescent treponemal antibodies.
The RPR (rapid plasma reagin) or V D R L
(Venereal Disease Research Laboratories) tests
are positive 100% of the time i n the secondary
stage of syphilis. However, these tests are positive o n l y 75% of the time i n untreated p r i m a r y
syphilis. The antibody appears 4 to 6 weeks
after the initial infection. If the initial tests are
negative, serologic tests should be repeated
3 months after the disease is suspected. D u r i n g
the secondary stage of syphilis, condylomata lata
may appear i n the perianal regin.
Treatment. Benzathine penicillin is the treatment of cholee for syphilis w i t h o u t central nervous system involvement. Altrnate treatments
30

include aqueous penicillin G, tetracycline, or


erythromycin.
Patients w i t h syphilis must abstain f r o m sexual contact u n t i l they are no longer contagious.
A l l contacts made d u r i n g the 3 months p r i o r to
diagnosis should be traced. Physical examinat i o n and serologic testing should be done every
3 months for 2 years foUowing treatment.
Herpes
Anorectal herpes, like genital herpes, is almost
always caused b y type I I herpes simplex virus
(HSV-2) although the H S V - 1 virus has occasionally been the causative agent. Previously
infected patients have antibodies to the specific
virus. These antibodies are present i n 20% to
50% of patients i n lower socioeconomic groups,
in about 10% of patients i n the upper socioeconomic groups, and in almost all older prostitutes.
Clinical features and diagnosis. The disease
usually presents w i t h perianal itching or paresthesias, followed by intense anal pain. The earliest visible lesions are small vesicles surrounded
by red areolas. The vesicle may rupture, leaving
an aphthous ulcer These lesions can appear on
the perianal skin, on the anoderm, and even on
the rectal mucosa. Secondary infection can result
in ulcerating cryptitis. Fever and malaise are
frequently present.
A f t e r a few days, the open lesions are covered
by a crust and healing occurs i n about 2 weeks.
A chronic relapsing course is c o m m o n , although
the recurrent lesions are usually m u c h less p a i n f u l than the initial ones.
Diagnosis is made b y viral culture, or material
f r o m the base of the r u p t u r e d vesicle can be
stained to show intranuclear inclusin bodies.
Treatment. There is no k n o w n cure for herpes.
Acyclovir as a topical 5% ointment may reduce
the length of the symptomatic p e r i o d . O r a l
acyclovir taken at the onset of symptoms can
reduce the f o r m a t i o n of new vesicles.
Patients are contagious while the lesions are
present and should abstain f r o m sexual activity
u n t i l all the lesions are completely healed. Even
after the lesions have completely healed, a cond o m should be used d u r i n g sexual intercourse.
PERIANAL A N D ANAL NEOPLASMS
Malignancies of the anal canal are u n c o m m o n ,
accounting for less than 5% of all anorectal cancers. The j u n c t i o n between rectal columnar epit h e l i u m and anal squamous e p i t h e l i u m occurs
gradually over a distance of 6 to 12 m m cephalad
to the dentate line. Columnar, cuboidal, transitional, and squamous e p i t h e l i u m are present i n
CLINICAL SYMPOSIA

this rea. The different types of epithelium in


this regin give rise to a variety of tumors.
Anal tumors arising above the dentate line
behave quite differently from tumors occurring
below this point, and it is helpful to categorize
these malignancies in relationship to the dentate
line. The World Health Organization has arbitrarily divided the anal canal into two regions,
calling the rea cephalad to the dentate line the
anal canal and the rea below this the anal margin.
Neoplasms of the A n a l Margin
Paget's disease. This disease is an uncommon
neoplasm that arises from the intraepidermal
part of the apocrine glands. Although Paget's disease of the nipple invariably overlies a mammary duct carcinoma, extramammary Paget's
disease is not necessarily associated with invasive cncer. However, the lesin should be considered premalignant. If left untreated, perianal
Paget's disease may eventually develop into an
adenocarcinoma. Patients with perianal Paget's
disease seem to be at high risk for developing
visceral carcinoma.
Severe, intractable itching is characteristic of
this disease. Clinically, the lesin appears to be
erythematous, scaly, and plaquelike. It occurs
most commonly in the elderly, and women are
affected more often than men. The diagnosis is
established by biopsy, which reveis the large,
pal, eccentrically nucleated Paget cells. A l l
scaly, pruritic anal lesions that do not heal
should be biopsied to rule out a neoplasm.
Treatment. Localized perianal Paget's disease is
treated by wide local excisin with clear margins
confirmed by microscopic examination. More
advanced lesions associated with an invasive
cncer require abdominal perineal proctectomy
A n inguinal lymph node dissection may also be
necessary to treat metastases. It is important to
follow these patients closely since other malignancies, especially cncer of the rectum and
breast, may develop.
Bowen's disease. This disease is a rare, slowgrovving intraepidermal squamous cell carcinoma (carcinoma in situ). It occurs most often in
the sixth or seventh decade of Ufe but may be
associated with condylomas in younger patients.
The lesin is usually a duU, brownish plaque but
may be nonpigmented. Ulceration usually indicates that an invasive carcinoma has developed,
a condition that occurs in about 10% of untreated
patients. A biopsy is required for diagnosis. In
addition to the histologic picture of squamous
cell carcinoma in situ, multinucleated giant cells
with vacuolated "halos" (Bowenoid cells) may be
VOLUME 37,

NUMBER 6

seen. Like Paget's disease, Bowen's disease is


associated with an increased incidence of visceral malignancies.
Treatment. These lesions should be treated by
wide local excisin, clear margins should be
confirmed microscopically Sometimes it is necessary to cover the excised rea with a splitthickness skin graft. Long-term foUow-up is
imperative not only because of the increased
risk of visceral malignancy but also because the
carcinoma in situ recurs locally in about 20%
of patients followed over 15 years.
Basal cell carcinoma. This carcinoma of the
anal margin is similar to basal cell carcinoma
occurring elsewhere on the skin. The lesin
presents as an ulcerated nodule with irregular,
elevated edges. Since these lesions do not metastasize, local excisin is the treatment of cholee. It
is important not to confuse the lesin histologically with basaloid carcinomas of the anal canaL
which are very malignant.
Squamous cell carcinoma. Arising candad to
the dentate line, squamous cell carcinoma has
characteristics similar to other squamous cancers
occurring elsewhere on the skin. The lesin is
frequently ulcerated with roUed, everted edges.
These lesions occur much more frequently in
men, whereas squamous cell carcinomas arising
above the dentate line are more common in
women.
These squamous ceU carcinomas are usually
well-differentiated keratinizing lesions, locally
invasive and late to metastasize. Because diagnosis is usually not made early, about 40% of
patients have metastases in the inguinal lymph
nodes.
Treatment. If the lesin is localized, wide excisin is the treatment of cholee. This procedure
often implies excising a portion of sphincteric
muscle to obtain adequate clearance, but this can
be done without loss of continence.
W h e n the cncer is deeply invasive and infiltrates sphincteric muscles, an abdominal perineal proctectomy is necessary If metastases are
found in the inguinal nodes, a groin dissection
should be performed. However, if the squamous
cncer does not invade the anal sphincters, twothirds of the patients treated by local excisin
survive 5 years. If inguinal nodes are involved at
the time of diagnosis, the 5-year survival rate is
less than 5%.
Neoplasms of the A n a l Canal
Squamous cell carcinoma. These malignant
lesions arise from the zone of transitional epithelium. There are several histologic variants of
31

these squamous t u m o r s , ncluding basaloid


carcinoma ( w h i c h has some histologic resemblance to basal cell carcinoma of the skin) a n d
m u c i n - p r o d u c i n g squamous carcinoma. C l i n i cally, these lesions e x h i b i t similar behavior A
l o n g h i s t o r y of m i l d anal p r o b l e m s w i t h b l e e d i n g or discharge is usual. Discovery of an anal
mass s h o u l d lead to biopsy, w h i c h c o n f i r m s the
diagnosis. A t the t i m e of diagnosis, these lesions
are f o u n d to metastasize to superior rectal nodes
in a b o u t half the patients and to i n g u i n a l nodes
in about o n e - t h i r d of patients.
Treatment. U n t i l recently, a b d o m i n a l perineal
resection was r e c o m m e n d e d as the treatment of
cholee. U n f o r t u n a t e l y , the cure rate f o U o w i n g
this procedure was less t h a n 50% i n most series.
A recently reported treatment for squamous
cell carcinoma of the anal canal used a c o m b i n e d
approach of i r r a d i a t i o n (3000 r delivered to
the pelvis over 3 weeks) f o l l o w e d b y a short
course of c h e m o t h e r a p y ( 5 - f l u o r o u r a c i l and
m i t o m y c i n - C ) . A b d o m i n a l perineal resection
was p e r f o r m e d 6 weeks after c o m p l e t i o n of
c h e m o t h e r a p y ; 5 of 9 patients had no residual
carcinoma detected i n the surgical specimen. A
similar approach, w i t h c h e m o t h e r a p y a d m i n i s tered p r i o r to i r r a d i a t i o n , has also been t r i e d .
A b o u t 2 or 3 weeks after c o m p l e t i o n of i r r a d i a t i o n , the lesin was excised. I n 4 of 10 patients,
no residual t u m o r was i d e n t i f i e d . These results
offer p r o m i s e of more effective treatment for
squamous cell cancers of the anal canal. If i n g u i nal metastases develop, t h e n an i n g u i n a l node
dissection s h o u l d be p e r f o r m e d . H o w e v e r , p r o phylactic node dissections are not r e c o m m e n d e d
because of the associated h i g h m o r b i d i t y
Adenocarcinoma. Carcinomas of the l o w e r
r e c t u m can extend d o w n w a r d a n d involve the

anal canal. A d e n o c a r c i n o m a can also arise f r o m


the anal ducts; these lesions present as a mass
residing beneath the surface of the anal e p i t h e l i u m . Rarely, adenocarcinoma m a y occur i n a
chronic anal fistula tract. These cases p r o b a b l y
represent p r i m a r y carcinomas of the anal d u c t
that have been misdiagnosed as anal fstulas.
A b d o m i n a l perineal resection is indicated
f o r anal adenocarcinoma, a n d some physicians
advcate the use of r a d i a t i o n therapy as an
a d j u n c t to surgery
Melanoma. T h e anal canal is the t h i r d most
c o m m o n site of m e l a n o m a , exceeded o n l y b y the
s k i n a n d eyes. S y m p t o m s are nonspecifc a n d
include bleeding, pain, and anal i r r i t a t i o n . A n a l
melanomas are u s u a l l y n o n p i g m e n t e d or l i g h t l y
p i g m e n t e d and are often confused w i t h more
benign lesions. Biopsy is necessary f o r diagnosis.
These lesions are extremely malignant, spreading submucosally as w e l l as b y l y m p h a t i c a n d
hematogenous routes. The t u m o r s are resistant
to c h e m o t h e r a p y a n d r a d i a t i o n . The o n l y hope
for cure is a b d o m i n a l perineal p r o c t o s i g m o i d ectomy p e r f o r m e d before metastases have
occurred. The cure rate is less t h a n 15%.
COMMENT
T h i s m o n o g r a p h is not meant to be a c o m p r e hensive treatise o n anorectal disease. W e have
tried to discuss the c o m m o n anorectal disorders
that a practicing physician encounters, e m p h a sizing our methods of treatment. W e realize that
in some instances other surgeons m i g h t advcate a somewhat different b u t equally effective
treatment. Nevertheless, it is o u r hope that this
m o n o g r a p h w i l l p r o v i d e practical and useful
i n f o r m a t i o n to beneft the u n f o r t u n a t e patients
afflicted w i t h anorectal disorders.

BIBLIOGRAPHY
Catterall RD. Sexually transmitted diseases of the anus
and rectum. Clin Gastroenterol 1 9 7 5 ; 4 : 6 5 9
Eisenstat T Salvati M D , Rubin RJ. The outpatient
management of acute hemorrhoidal disease. Dis Colon
Rectum 1 9 7 9 ; 2 2 : 3 1 5
Ferguson JA, Mazier WR, Ganchrow ML, et al. The
closed technique of hemorrhoidectomy Surgery
1971;70:480

Friend W G . The cause and treatment of idiopathic


pruritus ani. Dis Colon Rectum 1 9 7 7 ; 2 0 : 4 0
Fry RD. Office management of anal pain. Consultant
1985;25:134

Hanley PH, Ray JE, Pennington EE, et al. A ten-year


follow up study of horseshoe-abscess fistula-in-ano.
Dis Colon Rectum 1 9 7 6 ; 1 9 : 5 0 7
32

Hoffman MS, Kodner IJ, Fry RD. Internal intussusception of the rectum: Diagnosis and surgical management. Dis Colon Rectum 1 9 8 4 ; 2 7 : 4 3 5
MacLeod JH. Rational approach to treatment of hemorrhoids based on a theory of etiology Arch Surg
1983;118:29

Nigro N D , Vaitkevicius VK, Buroker T, et al. Combined therapy for cncer of the anal canal. Dis Colon
Rectum 1 9 8 1 ; 2 4 : 7 3
Parks AG, Gordon PH, Hardcastle JD. A classification
of fistula-in-ano. Br J Surg 1 9 7 6 ; 6 3 : 1
Ripstein CB, Lanter B. Etiology and surgical therapy of
massive prolapse of the rectum. Ann Surg 1 9 6 3 ;
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CLINICAL SYMPOSIA

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