The Pathogenesis of Hemorrhoids
PETER A. HAAS, M.D., THOMAS A. Fox, JR., M.D., GABRIEL P. HAAS, M.D.
Haas PA, Fox T A Jr, Haas G. T h e pathogenesis of hemorrhoids. Dis
Colon Rectum 1984;27:442-450.
The structure of the anal canal was examined in histology slides.
Hemorrhoids are normal features of the human anatomy. They are
pads that bulge into the lumen. Hemorrhoids have three parts: 1) the
lining, which Can be mucosa or anoderm; 2) the stroma with blood
vessels, smooth muscle, and supporting connective tissue; and 3) the
anchoring connective tissue system, which secures the hemorrhoids to
the internal sphincter and the conjoined longitudinal coat. T h e
anchoring and supporting connective tissue system deteriorates with
aging. T h e hemorrhoids not only bulge, hut descend into the lumen.
This becomes observable in the third decade of life, with individual
differences. T h e veins become distended as they lose their support. T h e
descended loose lining becomes more sensitive to pressure from strain-
ing and to trauma from the stool. There can be a stasis in the veins, with
clot formations and swelling, or erosions of the lining, with bleeding.
T h e hemorrhoids become symptomatic. [Key words: Hemorrhoids;
Etiology of hemorrhoids; Pathogenesis of hemorrhoids]
UNTIL RECENTLY, HEMORRHOIDSwere considered as
distended veins, much like the varicose veins of the legs or
esophagus. They are easily examined with endoscopes,
and anatomic and histologic studies can easily be per-
formed on autopsy specimens or surgically removed anal
canals or hemorrhoids.
Surgeons who operate on hemorrhoids know that they
are removing more than just distended veins, since bleed-
ing that occurs during surgery is more arterial than
venous. In recent years,l-4 some major theories have devel-
oped about the nature and causes of hemorrhoids. Ana-
tomic and hereditary factors have been mentioned, as well
as increased pressure within the anal canal. Nevertheless,
these theories do not explain why hemorrhoids or symp-
toms related to hemorrhoids are so rare in children and
y o u n g adults but occur frequently after the third decade of
life.
Are hemorrhoids normal or abnormal parts of the
h u m a n body? Are they abnormal only when they cause
symptoms? Are they present in older people only, or in all
Read at the meeting of the American Societyof Colon and Rectal
Surgeons, San Francisco, California, May 2 to 6, 1982.
Address reprint requests to Dr. Haas: Division of Colon and Rectal
Surgery, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit,
Michigan 48202.
442
From the Division of Colon and Rectal Surger 7,
Henry Ford Hospital, Detroit, Michigan
age groups? What is the anatomic composition of hemor-
rhoids, and are there any features that can explain the
symptoms? Is there any rational treatment of hemor-
rhoids based on the pathogenesis?
In this paper we compare our histologic, clinical, and
statistical findings with the data in the literature and try
to explain the nature and pathogenesis of hemorrhoids.
Materials and Methods
We e x a m i n e d the structure of the anal canal in 70
autopsy and surgical specimens taken from premature
newborns to patients over 80 years old. The specimens
were preserved in 10 per cent formaldehyde solution, and
histologic slides were made. T h e slides were stained with
hematoxylin and eosin, Masson trichrome, and Voerhoff-
vanGieson methods.S, 6 When we reviewed our slides, we
paid special attention to the submucosal and subcutane-
ous layers of the anal canal and the hemorrhoidal struc-
tures. We had certain technical difficulties in preparing
our slides. Because the lining of the anal canal in the
elderly is only loosely attached to the internal sphincter,
the mucosa was easily torn off during cutting. Although
this in itself is an important fact, we had to be very careful
in cutting the specimens and also in distinguishing
between the slackness of the attachments of the mucosa
and the artificially torn-off mucosa. Specimens taken
from the anal canals of infants and children presented no
such difficulties.
The Structure of Hemorrhoids
Hemorrhoids are located above or below the mucocu-
taneous junction of the anal canal. They bulge into the
lumen, sometimes protruding through the anal opening.
They are present in every age group from the newborn to
the elderly. T h e important parts of hemorrhoids are the
lining, the blood vessels surrounded by a connective
tissue stroma, and the anchoring system (Fig. 1). T h e
 Volume27
Number 7 HEMORRHOID PATHOGENESIS 443

FIG, 1. Cross-section of the anal canal in

a 2-year-old girl. H e m o r r h o i d is bulging,
but not descending into the anal canal.
Firm connective tissue fibers s u p p o r t the
blood vessels in the hemorrhoid and anchor
it to the internal sphincter and longitu-
dinal coat (van Gieson; original magnifi-
cation X8).

444
hemorrhoids are covered by mucosa (internal hemor-
rhoids) or anoderm (external hemorrhoids).
In the young, under normal circumstances, only inter-
nal hemorrhoids bulge into the lumen. However, starting
in the third decade of life, internal hemorrhoids descend
into the lower part of the anal canal, and the external
hemorrhoids also start to bulge. By looking at the lining
of protruding hemorrhoids, one can tell if they are inter-
nal or external. The mucocutaneous junction, can also
descend. Sometimes, small defects in the skin or mucosa
can bleed from eroded blood vessels. So far, we have found
no evidence that these erosions make hemorrhoids more
vulnerable to bacterial invasion and infection, but our
present studies are not sufficient to determine this
conclusively.
Blood vessels under the nmcosa or anoderm sur-
rounded by connective tissue form the bulk of the hemor-
rhoids, sometimes called " c u s h i o n s . ''~ T h e arteries and
veins are in close proximity. In the young, connective
Dis. Col. 8e Rect.
HAAS, E T AL. July 1984
tissue fibers seem to support the blood vessels, they are
dense, well organized, and parallel to each other (Fig. 9).
Around age 30, the connective tissue fibers start to disin-
tegrate; they loosen around the blood vessels, and the
veins become distended (Fig. 3). Blood clot formation,
particularly in external hemorrhoids, is common. Smooth
muscle fibers without any regular pattern are present in
the hemorrhoids, as well as in the submucosa and subcu-
taneous layer.
The connective tissue fibers of hemorrhoids are exten-
sions of the submucosa fibers. They are mainly collage-
nous in nature; however, many elastic fibers appear in the
submucosa of the very young. T h e collagen fibers of the
submucosa anchor the hemorrhoids and anal mucosa to
the internal sphincter. T h e connective tissue fibers con-
tinue laterally between the smooth muscle fibers: the
mucosa and hemorrhoids are anchored to the fibers of the
conjoined longitudinal coat of the anal canal (Fig. 4).
In younger age groups, collagen fibers anchor the anal
FIG. 2. Well organized dense fibers in
the submucosaof a 9-year-oldboy (Masson
trichrome; original magnification )<40).
Volume 27
Number 7 HEMORRHOID
mucosa and hemorrhoids firmly to the internal sphincter
and to the longitudinal coat. In older age groups, the
anchoring connective tissue system degenerates and the
fibers are broken loose. The hemorrhoids are detached
from the internal sphincter and slide downward. The
anoderm also becomes loose and bulges into the anal
canal or around the anal opening (Fig. 5).
Discussion
Many physicians and almost every lay person consider
hemorrhoids to be a pathologic condition. While hemor-
rhoids are very c o m m o n , only a relatively small number
of people have symptoms related to hemorrhoids. Review-
ing the reports of 835 rectal examinations, we found that
the prevalence of hemorrhoids is almost identical in
patients of every age group, whether or not they have
symptoms related to hemorrhoids. 7 We concluded that
hemorrhoids are normal parts of the h u m a n anatomy.
FIG. 3. Connective tissue fibers in this
28-year-oldman are not as denseas in Fig-
ure 2. They do not support the blood ves-
sels (Masson trichrome; original magnifi-
cation •
PATHOGENESIS 445
Although everybody, or almost everybody, has hemor-
rhoids, there are still notable differences in the size of
hemorrhoids and whether they are asymptomatic or have
symptoms such as bleeding, protrusion, blood clot for-
mation, etc. Anatomic factors may explain the presence of
hemorrhoids in the entire population, whereas hereditary
and environmental factors and individual habits are
responsible for the different presentation or symptoma-
tology of hemorrhoids in different groups or individuals.
Important textbooks 8,9 discuss hemorrhoids as dis-
tended veins and consider stasis from various causes, such
as portal hypertension or carcinoma, as an etiologic fac-
tor. Graham-Stewart and Burkit0~ n describe hemor-
rhoids as distended veins caused by straining during
defecation. Evidence does not support the theory that
portal hypertension can cause hemorrhoids. Jacobs e t
a l. 12 found that the incidence of hemorrhoids in patients
with portal hypertension is not increased above that
expected in the population at large. Hirschowitz 13 states
 446 HAAS, ET AL.
that hemorrhoids do not necessarily occur in patients
with esophageal varices. Swart 14stated that because of the
long distance between the portal and hemorrhoidal veins,
based on the Hagen-Poisseuill equation, venous pressure
in the hemorrhoids does not increase appreciably, and
they are not an important site of collateral circulation
between the vena cava and portal system.
In 1919 Miles 15 described the anatomy of the end
branches of the superior hemorrhoidal artery. They ter-
minate in the submucosa just above the dentate line with
an anterior and posterior branch on the right side, and a
single on the left. Miles called these sites the "primary
piles." T h e right posterior and the left branches give off
two end branches anteriorly and posteriorly, which are
the sites of the "secondary piles." T h e arterial end
branches supply the hemorrhoidal venous plexus with
blood. T h e end branches can be easily palpated at rectal
examination. Hence, the bleeding encountered during
hemorrhoidectomy is more arterial than venous.
Dis. Col. ~ Rect.
July 1984
FIG. 4. Connective fibers anchor the
mucosa and submucosa to the internal
sphincter and penetrate between the fibers
of the sphincter to the conjoinedlongitud-
inal coat in this 9-year-old girl (Masson
trichrome; original magnification X19).
Steltzner I explained the arterial bleeding by describing
arteriovenous anastomoses (A-V shunts) in the hemor-
rhoidal plexus in what he called "corpus cavernosum
recti." He also felt that these corpora have an important
role in anal continence. Thulesius and Gj6res 16 proved
the existence of A-V shunting by studying the oxygen
content of hemorrhoidal blood, while T h o m s o n ~demon-
strated the presence of A-V shunts with an injection
technique.
Present probably fiom birth, A-V shunts are c o m m o n
under the mucosa of the entire intestinal tract. However,
if A-V shunts are responsible for hemorrhoidal symptoms
in adults, infants or children should also have symptoms.
In 1975 T h o m s o n z described thickenings of the anal
submucosa that he called "cushions." The cushions are
composed largely of blood vessels, smooth muscle, and
elastic and collagen connective tissue. There are three
main cushions: the left lateral, right anterior, and right
posterior. T h e venous plexus was found to be congre-
Volta'he 27
Number 7 HEMORRHOID
FIG.5. Connectivetissue fibersare loose
and broken in a 70-year-oldman. They do
not support and anchor the blood vessels
and anoderm (Masson trichrome; original
magnification X13.5).
gated within the cushions, not forming a uniform net-
work around the anal canal. T h e cushions are formed in
embryonic life and contribute to the mechanism of anal
closure. Irregular bowel habits, straining, and hard and
bulky stool would exert pressure on the cushions. Hemor-
rhoids are the result of the downward displacement of the
cushions.
O u r studies confirm T h o m s o n ' s findings. Hemor-
rhoids are the thickenings of the submucosa, composed of
b l o o d vessels a n d connective tissue stroma, covered by
mucosa. T h e "cushions" are anchored by collagen con-
nective tissue fibers to the internal sphincter and to the
conjoined longitudinal coat.
T h e connective tissue fibers that anchor the mucosa
and the hemorrhoids are dense, firm, and intact in the
young, and weak, disintegrated, loose, and broken in
older individuals. O u r studies and others ~7confirmed that
these pads are present in the embryo (Fig. 6). Changes in
the connective tissue system are signs of aging, as happens
PATHOGENESIS 447
also in other parts of the body. 6 T h e weakened connective
tissue fibers are not able to anchor the anal mucosa, skin,
and hemorrhoids against the downward active forces in
the anal canal. As the cushions are displaced downward,
the external hemorrhoids start to bulge inside and outside
of the anal canal.
Gass a n d Adams TM pointed out, in 1950, that the out-
standing feature of hemorrhoids is the loose, fragmented
nature of the collagenous connective tissue, which has
lost its usual compact architecture. In 1965 Jackson and
Robertson 19reported that the high degree of elastic tissue
seen in infants and older children fragments and gradu-
ally degenerates in hemorrhoidal disease. Although sim-
ilar changes occur with advancing age in other organs,
they believe that the breakdown of the connective tissue is
the consequence of the daily trauma of straining. Others
attribute the breakdown of the connective tissue to the
shearing force of fecal bolus, which causes stretching, z~
T h e theory of aging explains the deterioration of the

448
FIG. 6. Cross-section of the anal canal in a newborn girl. Three primary hemorrhoidal pads a n d secondary pads bulge into the lumen. T h e y are
firmly anchored by dense connective tissue fibers (van Gieson; X21).
anchoring connective tissue better than the "wear and
tear" theory. In 1963 Strehler 21 stated that fibers and cells
of the connective tissue become disorganized with ad-
vancing age, and Bornstein 22described age-related changes
in collagen synthesis. Age-related changes in the collage-
nase function may also possibly degrade native collagen.
T h e smooth muscle elements in the anal submucosa
are called the muscle of TreitzZ or muscularis submuco-
sae. 23These muscle fibers do not seem to have any regular
pattern; they are m u c h less numerous than the connective
tissue fibers and, except for their presence, there is no
evidence that they have any role in anchoring the mucosa.
We believe that these smooth muscle fibers may more
likely be aberrant elements of the internal sphincter
muscle.
Within age groups hemorrhoids differ in size. The
hemorrhoids of certain individuals start to descend at an
earlier age, whereas for others the sagging starts later.
Hemorrhoids can increase or decrease in size in a given
individual from time to time, 24 but only within a rela-
tively short period. Miles ~5 correctly states that during a
lifetime, "hemorrhoids are inevitably progressive." Some
evidence indicates that hereditary factors may play a role, 4
but further investigations are necessary.
Dis. Col. geRect.
HAAS, E T AL. July 1984
The role of environmental factors is well established.
Burkitt 3 pointed out the role of the low-fiber diet in the
pathogenesis of hemorrhoids. No doubt, constipation,
repeated and prolonged straining, and hard stool can
produce symptoms of hemorrhoids, such as sagging of
the "cushions"; and the external hemorrhoids can be
exaggerated. Prolonged venous stasis can dilate the
venous sinuses if they are not protected by a strong con-
nective tissue stroma. Small inj uries of the mucosa or skin
may result in bleeding, etc. Whatever poor eating habits a
large g r o u p of people or an individual may have, eating
habits are the same a m o n g children, y o u n g adults, and in
the elderly as a group. There is no evidence that in West-
ern cultures children eat more fiber than adults, although
the prevalence of hemorrhoids is low in children and
high in adults. However, an individual's eating and
bowel habits can deteriorate over a lifetime and pre-
viously asymptomatic hemorrhoids can cause symptoms.
But hemorrhoids, symptomatic or asymptomatic, start to
sag when the anchoring system begins to deteriorate in
the third decade of life.
Other theories also attempt to explain the etiology of
hemorrhoids. Nesselro& 5 thinks that the principal factor
in the pathogenesis of hemorrhoids is anal infection,
Volume 27
Number 7 HEMORRHOID
while McGivney 26 has been impressed by the high inci-
dence of round cell infiltration in the tissues immediately
adjacent to the anal crypts. McGivney also noted changes
in the connective tissue fibers supporting the blood ves-
sels, but he attributed these changes to the infectious
process.
Hansen 27 examined the venous outflow of the anal
canal. H e thinks that forceful and sometimes unsuccess-
ful straining causes compression of the venous system
and stasis in the "corpora cavernosa," with dilatation of
the venous sinuses. L o r d 28 tried to renew the interest in
the "pecten band," which is the lower border of the
internal sphincter. In certain individuals the muscle
becomes hypertrophic, and the anal outlet narrows. At
straining, the vascular "cushions" descend through the
narrow outlet, and they are nipped, which leads to symp-
toms. While L o r d recommended forceful dilatation to
overcome the narrowness, Eisenhammer ~9 believes that
the narrowness begins with a sphincter spasm that later
becomes anatomic, and that the proper treatment is
sphincterotomy.
Most of these theories have some validity. It is certain
that the pads are present at the embryonic stage of devel-
opment. Although there are more than three pads, the
i m p o r t a n t locations are right anterior, right posterior,
and left lateral, corresponding to the end branches of the
superior hemorrhoidal arteries. There can be little doubt
that arteriovenous shunts are present in the vascular ele-
ments of the pads. It seems certain that the supporting-
anchoring connective tissue system deteriorates during
the lifetime due to aging. Because the tissue can no longer
support the blood vessels or anchor the pads, the vessels
become distended and the pads are dislocated downward.
T h e speed and degree of aging of the connective tissue
system can be hereditary. I m p r o p e r diet (which can cause
constipation), frequent straining, hard stool, and chronic
use of laxatives may increase the downward pressure and
exaggerate the sagging of the hemorrhoids. Narrowness
of the anal canal may facilitate injuries of the mucosa and
skin of the anal canal, causing bleeding. If increased
pressure acts at the weak pedicle of the hemorrhoids, it
can cause stasis, edema, and blood clot formation.
Hemorrhoids are normal anatomic structures present in
every individual. T h e y do not need treatment. H e m o r -
rhoidal s y m p t o m s or symptomatic hemorrhoids are
abnormal conditions that may need preventive care and
different types of treatment.
Summary
Hemorrhoids are n o r m a l features of the h u m a n anat-
omy. T h e y are pads that bulge into the l u m e n of the anal
canal. T h e y have three i m p o r t a n t parts: 1) the lining,
which can be mucosa or anoderm; 2) the stroma with
blood vessels, smooth muscle elements, and s u p p o r t i n g
PATHOGENESIS 449
connective tissue--the vessels form arteriovenous shunts
- - a n d 3) the anchoring connective tissue system, which
secures the hemorrhoids to the internal sphincter and the
conjoined longitudinal coat.
As an individual ages, the anchoring and supporting
connective tissue system deteriorates, and the hemor-
rhoids not only bulge but also descend into the lumen of
the anal canal. T h i s change becomes apparent clinically
or observable endoscopically in the third decade of life,
with certain individual differences. T h e veins also become
distended as they lose their support.
T h e descended loose lining of the hemorrhoids and the
weakened pads become more exposed and sensitive to
increased pressure from straining and to trauma from the
hard stool. There will be a stasis in the blood vessels, with
occasional clot formations or swelling, and erosions of
the lining and the vessel walls, with bleeding. Thus,
hemorrhoidal symptoms or hemorrhoidal disease can
occur.
References
1. Stelzner F. DieH~imorrhoiden undandereKrankheitendesCorpus
cavernosum recti und des Analkanals. Dtsch Med Wchnschr
1963;88:689-96.
2. Thomson WH. The nature of haemorrhoids. Br J Surg 1975;
62:542-52.
3. Burkitt DP. Hemorrhoids, varicose veins and deep vein thrombo-
sis: epidemiologic features and suggestive causative factors. Can
J Surg 1975;18:483-8.
4. Brondel H, Gondran M. Facteurs pr6disposants li6s a l'h~r~dit6 et
a la profession dans la maladie h6morroi'daire. Arch Fr Mal App
Dig 1976;65:541-50.
5. Haas PA, Fox TA Jr. The importance of the perianal connective
tissue in the surgical anatomy and function of the anus. Dis
Colon Rectum 1977;20:303-13.
6. Haas PA, Fox TA Jr. Age-related changes and scar formations of
the perianal connective tissue. Dis Colon Rectum 1979;23:160-9.
7. Haas PA, Haas GP, Schmaltz S, Fox TA. The prevalence of hemor-
rhoids. Dis Colon Rectum 1983;26:435-39.
8. Ackerman LV, Butcher HR. Surgical pathology. 3rded. St. Louis:
CV Mosby, 1969.
9. Anderson WA. Pathology. 5th ed. St. Louis: CV Mosby, 1966.
10. Graham-Stewart CW. What causes hemorrhoids? A new theory of
etiology. Dis Colon Rectum 1963;6:333-44.
11. Burkitt DP, Graham-Stewart CW. Haemorrhoids--postulated
pathogenesis and proposed prevention. Postgrad Med J 1975;
51:631-6.
12. Jacobs DM, Bubrick MP, Onstad GR, Hitchcock CR. The rela-
tionship of hemorrhoids to portal hypertension. Dis Colon Rec-
tum 1980;23:567-9.
13. Hirschowitz B. Medical Grand Rounds, University of Alabama
Center. South Med J 1969;62:266-74.
14. Swart B. lJberlegungen zur Genese typischer Kollateralkreislanfe
bei portalem Hochdruck und deren r6ntgenologisch-klinische
Symptomatologie. Radiologe 1968;8:73-83.
15. Miles WE. Observations upon internal piles. Surg Gynecol Obstet
1919;29:497-506.
16. Thulesius O, Gj6res JE. Arterio-venous anastomoses in the anal
region with reference to the pathogenesis and treatment of
hemorrhoids. Acta Chir Scand 1973;139:476-8.
17. Wilson PM. Anorectal closing mechanisms. S Aft" Med J 1977;
51:802-8.
18. Gass OC, Adams J. Hemorrhoids: etiology and pathology. Am J
Surg 1950;29:40-3.
 Dis. Col. & Rect.
450 H A A S , E T AL. July 1984

19. Jackson CC, Robertson E. Etiologic aspects of hemorrhoidal dis-
ease. Dis Colon Rectum 1965;8:185-9.
20. Tagart REB. Haemorrhoids and palpable ano-rectal lesions. Prac-
titioner 1974;212:221-38.
21. Strehler BL. Time, cells and aging. New York: Academic Press,
1963;138-45,
22. Bornstein P. Disorders of connective tissue function and the aging
process: a synthesis and review of current concepts and findings.
Mech Ageing Dev 1976;5:305-14.
23. Fine J, Lawes CHW. On the muscle fibers of the anal submucosa
with special reference to the pecten band. Br J Surg 1940;
27:723-7.
24. Collopy BT. Internal haemorrhoids: observations on their nature
and classification in relation to their management, Aust NZ J
Surg 1980;50:167-9.
25. Nesselrod JP. Hemorrhoids (letter to Editor). Arch Surg 1974;
109:458.
26. McGivney J, A reevaluation of etiologic factors of hemorrhoidal
disease. Ariz Med 1967;24:333-6.
27. Hansen HH. Neue Aspekte zur Pathogenese und Therapie des
Hfimorrhoidalleidens. Dtsch Med Wchnschr 1977;102:1244-8.
28. Lord PH. Approach to the treatment of anorectal disease with a
special reference to hemorrhoids. Surg Annu 1977;9:195-9.
29. Eisenhammer S. Internal anal sphincterotomy plus free dilatation
versus anal stretch with special criticism of the anal stretch
procedure for hemorrhoids: the recommended modern approach
to hemorrhoid treatment. Dis Colon Rectum 1974;17:493-522.

Announcement

70TH ANNUAL CLINICAL CONGRESS

T h e 70th a n n u a l C l i n i c a l Congress of the A m e r i c a n College of Surgeons

will be held in San Francisco, October 21-96, 1984. M o r e t h a n 10,000
p h y s i c i a n s are expected to register for the Congress, w i t h total attendance,
i n c l u d i n g guests, o t h e r medical professionals, a n d scientific a n d i n d u s t r i a l
exhibitors, exceeding 20,000. C o - h e a d q u a r t e r s for the C o n g r e s s will be the
M o s c o n e C o n v e n t i o n Center, the F a i r m o n t Hotel, a n d t h e San F r a n c i s c o
H i l t o n a n d Towers. Scientific a n d technical e x h i b i t i o n s will be located in
the M o s c o n e C o n v e n t i o n Center. P o r t i o n s of the scientific p r o g r a m will
take place in the Moscone C o n v e n t i o n Center, as well as the F a i r m o n t , San
Francisco H i l t o n , a n d W e s t i n St. Francis hotels. T h e m a i n registration area
d u r i n g the week of the Congress will be in the M o s c o n e C o n v e n t i o n Center.
T h e r e will also be advance registration desks at the F a i r m o n t Hotel, the San
Francisco H i l t o n a n d Towers, a n d the W e s t i n St. Francis H o t e l o n Sunday,
October 21 only. Due to space l i m i t a t i o n s , nurses, medical students, a n d
allied h e a l t h professionals m a y register to a t t e n d o n l y those scientific ses-
sions t h a t will be held in the M o s c o n e C o n v e n t i o n Center. T h e y m a y also
tour the scientific a n d technical e x h i b i t areas w i t h o u t a d d i t i o n a l charge.
T h e A m e r i c a n College of S u r g e o n s is accredited by the Accreditation C o u n -
cil for C o n t i n u i n g Medical E d u c a t i o n to s p o n s o r c o n t i n u i n g medical edu-
cation for physicians. T h e College designates that this c o n t i n u i n g medical
e d u c a t i o n offering also meets the criteria for h o u r - f o r - h o u r credit i n Cate-
gory I as o u t l i n e d by the A m e r i c a n Medical Association for the P h y s i c i a n ' s
R e c o g n i t i o n Award. R e g i s t r a t i o n fees for the C l i n i c a l Congress are waived
for Fellows of the College w h o s e dues are p a i d for 1983 a n d for Initiates a n d
p a r t i c i p a n t s i n the C a n d i d a t e G r o u p . T h e r e g i s t r a t i o n fee for n o n - F e l l o w s
is $255. Surgical residents w h o b r i n g a letter verifying t h e i r residency status
may register for $125. P a r t i c i p a n t s w h o e n r o l l in p o s t g r a d u a t e courses,
i n c l u d i n g those whose registration for the Congress is free, m u s t pay t h e
a p p r o p r i a t e fees for the courses selected. For f u r t h e r i n f o r m a t i o n , contact
L i n n Meyer or K a t h r y n J o r d a n , 55 East Erie Street, C h i c a g o , Illinois 60611.
T e l e p h o n e (312) 664-4050.