Декабрь

Coloi'eetal
Disease
Int J Colorect Dis (1988) 3:191 194
9 Springer-Verlag 1988
Original articles
Evaluation of perineal descent by defaecography
E. Skomorowska, V. Hegediis and J. Christiansen
Department of Surgery D and Department of Radiology, Glostrup Hospital, University of Copenhagen, Copenhagen, Denmark
Abstract. Perineal descent was studied by defaecography with the patients in the sitting position in
55 healthy volunteers, 21 women with idiopathic
faecal incontinence and 8 women with obstructed
defaecation. This technique provides data necessary for the evaluation of defaecation disorders, i.e.
morphological changes during defaecation as well
as the dynamics of the pelvic floor. It was found
that the pelvic floor position during rest and during
straining is almost the same in women with incontinence and in women with obstructed defaecation.
Furthermore patients with normal position of the
pelvic floor during rest may exhibit considerable
descent during straining while patients with abnormal position of the perineum during rest may show
normal descent during straining. This observation
may indicate that the first sign of abnormal function may be an increased descent during straining,
only later following by descent during rest. The
importance of establishing control data is emphasized since differences in defaecographic techniques
between different centres may render comparison
difficult.
Perineal descent is often present both in patients

with anal incontinence and obstructed defaecation
(outlet obstruction) [1, 2], and the surgical treatment of these conditions will in most cases have to
include a procedure which reduces perineal descent.
The position of the perineum should be studied
with the subject in the sitting position in order to
mimic physiological conditions, since a different
perineal position and movement on straining is
seen when the subject is studied in the horizontal
position [2-6]. Detailed measurements of perineal
descent during defaecography have not been done
in previous studies [6-8]. We describe a technique
employing a combination of static and dynamic

tests which allows evaluation of the position and
movement of the pelvic floor during rest and straining. This method has in a previous publication been
used for evaluation of dynamic rectal pathology
(internal intussusception, prolapse, rectocele,
recto-sacral separation) and for measuring of the
anorectal angle [9, 10].
Material and methods
Fifty-five healthy volunteers, 30 women (median age 54 years,
range: 4 1 - 7 4 ) and 25 males (58 years, 38-71), 21 women with
idiopathic faecal incontinence (59 years, 25-82) and 8 women
with a history of obstructed defaecation (47 years, 2 9 - 8 3 ) were
studied.
The control subjects were patients without defaecation disorders who for other reasons had been referred for a barium
enema. The CD examination was performed on the same day
and prior to the barium enema. Only those patients in whom the
barium enema did not reveal any pathology were included in the
series. Informed consent was obtained from all subjects.
Technique
Approximately 200 ml of a thick barium contrast medium (a
mixture of equal volumes of Mixobar oesophagus | and Mixobar suspension | were instilled through a catheter into the rectum. After the instillation the catheter was removed so that the
anal canal was marked with contrast, as published by others [6].
The subject was then placed on a commode in front of a fluoroscopic unit, with the lateral view of the rectum positioned in the
centre of the field. All stages of defaecation were registered on
videotape and static images were taken at rest and during maximum straining. The x-ray machine used had a film-focal distance of 120 cm. The magnification of midline structures (rectum, anus) were measured using a metallic p h a n t o m to 3 m m
on average in the neighbourhood of the central beam.
Evaluation (Fig. 1)
Measurement of the position of the pelvic floor (perineal descent) at rest (DR) was done on the static images. D R is defined
192
Rest
DS-R
cm
Strain
10
8"
oo
6-
4Fig. 1. Measurement of pelvic floor position at rest (DR) and at

strain (Ds_g)
el
_
__.,_:.~"
"___
ee
eooOoooo
eel
o~o
eel
-'-:~eo~o
ee
eoeo
oo
2-
6o
asymptomatic
asymptomatic
male
female
volunteers
volunteers
Fig. 4. Descent of the pelvic floor during straining (Ds_~) in
asymptomatic control subjects
DR
cm
,4
o e o o o o o
II
ooooo
Table 1. Additional pathology revealed by the defaecography in

women with faecal incontinence or outlet obstruction
+2II
0Incontinence
Outlet
obstruction
6
3
7
5
21
1
5
0
2
8
-2-
asymptomatic
asymptomatic
male
female
volunteers
volunteers
Fig. 2. Resting pelvic floor position (DR) in relation to the ramus ossis ischii (cm) in asymptomatic control subjects
DR
cm
*4
+2-
None
Rectal intussusception
Rectal prolapse
Rectocele
Total
Results
oo
o o o o o
go
e o o o
o o e o e e
--:::;:::--
O-
el
--o--I-I--
::.
asymptomatic
incontinence outlet obstruction
Fig. 3. Resting pelvic floor position

incontinence and outlet obstruction
(DR) in women
with faecal
as the distance in cm of the an 9

junction above ( + ) or
below (-) the lower edge of the ramus ossis ischii measured at
rest. Ds_ R is the difference in cm between the level of the pelvic
floor (the an 9
junction) at rest and during maximum
straining. For this measurement the edge of the commode served
as reference point since in some patients perineal descent during
straining was so pronounced that the an 9
junction and the
ramus ossis ischii were not visible on the video screen at the same
time. Results are given as median with range (r) and 95% confidence limits (cf). Differences were assessed by the M a n n Whitney test and values less than 0.05 were considered significant.
The resting pelvic floor position in relation to the

ramus ossis ischii (DR) in asymptomatic women
was + 2 . 0 c m (r: + 1 . 0 - - + 4 . 5 ) ; cf: + 1 . 5 - - + 2 . 5 )
and in asymptomatic males +2.5 (r: + 1.0 -- +4.0;
cf: + 2.0 - + 3.0); (p = 0.04) (Fig. 2).
Females with faecal incontinence had a median
D~ of 0 cm (r: - 4 . 0 - +2.0; cf: - 2 . 5 - 0 ) , which is
significantly lower than found in the control group
(p < 0.01). Women with outlet obstruction also had
a D R of 0 c m (r: - 1 . 5 - + 2 . 5 ; cf: - 1 . 0 - + 2 . 5 )
also significantly lower than the control group
(p<0.001) (Fig. 3).
The descent of the pelvic floor during straining,
i.e. the difference in the position of the an 9
junction at rest and during maximum straining
(Ds-R) was in asymptomatic women 4.5cm
(r: 1.5-8.0; cf: 3.5-5.5) and in asymptomatic males
4.0 cm (r: 2.0-7.5; cf: 3.0-5.0); (p >0.10) (Fig. 4).
Women with faecal incontinence had a D s R of
7.0 cm (r: 2.0-13.0; cf: 4.0-9.0), and women with
outlet obstruction 10 cm (4.5-13.0; cf: 8.0-13.0),
both groups significantly greater than the control
group (p < 0.02). Descent during straining was sig-
193
DS-R
cm
14
1210-
8- -
- -
e - e - ~ - -
nificantly greater in women with outlet obstruction

than in incontinent women (p = 0.025).
Table 2 shows that a number of incontinent
women have a normal pelvic floor position at rest
(DR) but an abnormal descent during straining
(Ds_R). The same is true for women with obstructed defaecation (Table 3).
- -
6ee*
-- --o-r
4-
~176
Discussion
o 9
ooo
o00*
o9
2-
asymptomatic
incontinence outlet obstruction
Fig. 5. Descent of the pelvic floor during straining (Ds_R) in

asymptomatic women and women with faecal incontinence and
outlet obstruction
Table 2. Pelvic floor position at rest (DR) and during straining

(Ds- R) in 21 female patients with anal incontinence
DR, cm
DS_R, cm
+1
+2
+2
+1.5
2
-2
-2
-3
-2.5
3
0
0
0
0
0
0
0
-3
-1.5
2.5
10
7
7
7
4.5
4
4
3
2
4.5
3
8
9
8
8
13
8.5
10
13
10
Table 3. Pelvic floor position at rest (DR) and during straining
(Ds_R) in 8 female patients with outlet obstruction

DR, cm
DS_R, cm
+2.5
+1
+1
0
0
0
-1
-1.5
13
13
13
9
9
8
4.5
11
Defaecography with the technique used in this

study provides a number of data necessary for the
evaluation of defaecation disorders in a single
examination. In most studies where defaecography
has been used, only the morphological changes
during defaecation have been examined [1, 7]. In
some studies anorectal angle but not pelvic floor
descent were measured [6, 8], while measurement of
perineal descent, if performed, was done in a separate examination using standard X-ray technique,
often with the patient in the horizontal position [3,
4].
In previous studies on the position of the pelvic
floor during straining [9, 10] we did not relate it to
the position during rest, but according to our present experience, pelvic floor descent can only be
evaluated by comparison of the movement of the
perineum during straining with its original position
during rest.
From the present study it appears that there is
a small but significant difference in the position of
the pelvic floor during rest between the sexes. During straining, however, no such difference was
found.
Since there is no universal agreement as to the
technical procedure for defaecography, values for
pelvic floor descent obtained in different centres
vary considerably [2, 3]. Position of the pelvic floor
in relation to the ramus ischii during straining measured by Henry et al. [5] are not comparable with
those found in this study, probably because of difference in procedure. One difference is that these
authors examined the patients in the horizontal
position in which maximum straining cannot be
obtained, whereas our results were obtained during
straining in the sitting position resulting in a greater
descent. Similarly the difference in descent during
straining between control subjects and patients was
smaller than observed by us, and they did not find
any difference in the position of the perineum between control subjects and patients at rest.
This indicates that unless the same technique is
used in different centres, each centre has to collect
194
its o w n c o n t r o l d a t a before m e a s u r e m e n t s can be
used to identify p a t h o l o g i c a l conditions. This is
f u r t h e r m o r e e m p h a s i z e d b y considerable overlap
between values for n o r m a l individuals a n d patients
in this study. E s t a b l i s h m e n t o f confidence intervals
for control d a t a m a k e s identification o f p a t h o l o gical conditions easier a n d m o r e reliable.
O u r study shows t h a t the p a t h o l o g i c a l values
for pelvic floor position during rest (DR) a n d during straining (Ds_R) are a l m o s t similar in w o m e n
with incontinence a n d w o m e n with outlet obstruction. This is in a g r e e m e n t with previous o b s e r v a tions t h a t pelvic floor descent is p r o b a b l y an i m p o r t a n t c o m m o n p a t h o g e n e t i c factor, which clinically
can present either as incontinence or as outlet obstruction [1]. We f o u n d t h a t some patients with
n o r m a l position o f the pelvic floor during rest
showed increased descent during straining; this was
seen in 37% o f the patients with outlet o b s t r u c t i o n
versus 19% in patients with incontinence. Likewise
s o m e patients with a b n o r m a l position o f the pelvic
floor during rest showed n o r m a l descent during
straining; this was seen in 3 3 % o f patients with
incontinence versus 12% o f patients with outlet
obstruction. These findings indicate t h a t the first
sign o f a pelvic floor a b n o r m a l i t y m a y be increased
descent during straining, only later followed by
descent at rest, indicating t h a t incontinence m a y be
the end result o f o b s t r u c t e d defaecation.
In conclusion d e f a e c o g r a p h y p e r f o r m e d with
the technique described here gives i n f o r m a t i o n n o t
only on the m o r p h o l o g i c a l changes during defaecation but also on the d y n a m i c state o f the pelvic
floor. The i m p o r t a n c e o f establishing reliable control d a t a is emphasized.
References
1. Berman JR, Manning DM, Dudley-Wright K (1985) Anatomic specificity in diagnosis and treatment of internal
rectal prolapse. Dis Colon Rectum 28:816-826
2. Parks AG, Porter NH, Hardcastle J (1966) The syndrome of
the descending perineum. Proc R Soc Med 59:477-482
3. Bartolo DCC, Read NW, Jarratt JA, Read MG, Donnelly
TC, Johnson AG (1983) Differences in anal sphincter function and clinical presentation in patients with pelvic floor
descent. Gastroenterology 85:68 75
4. Bartolo DCC, Roe AM, Virjee J, Mortensen NJMcC
(1985) Evacuation proctography in obstructed defaecation
and rectal intussusception. Br J Surg 72:111-116
5. Henry MM, Parks AG, Swash M (1982) The pelvic floor
musculature in the descending perineum syndrome. Br J
Surg 69:470 472
6. Mahieu P, Pringot J, Bodart P (1984) Defecography: I.
Description of new procedure and results in normal patients. Gastrointest Radiol 9:247-251
7. Broden B, Snellman B (1968) Procidcntia of the rectum
studied with cineradiography. A contribution to the discussion of causative mechanism. Dis Colon Rectum 11: 330- 347
8. Mahieu P, Pringot J, Bodart P (1984) Defecography: II.
Contribution to the diagnosis of defecation disorders. Gastrointest Radiol 9:253 261
9. Mahieu PHG (1986) Defecography in anorectal defecation
disorders. First Biennal Congress of European Council of
Coloproctology, Bologna
10. Skomorowska E, Henrichsen S, Christiansen J, Hegedfis V
(1987) Videodefaecography combined with measurement of
the anorectal angle and perineal descent. Acta Radiol Diagn
28:559-562
11. Skomorowska E, Hegediis V (1987) Sex differences in anorectal angle and perineal descent. Gastrointest Radiol
12:353-355
Accepted: 17 June 1988
Dr. John Christiansen
Department of Surgery D
Glostrup Hospital
DK-2600 Copenhagen
Denmark
Col6i'ec/al
Disease
Int J Colorect Dis (1988) 3:195-200
Rectal cancer: factors influencing the development

of local recurrence after radical anterior resection
W. Feil 1, M. Wunderlich z, E. Kovats 1, N. Neuhold 2, M. Schemper 1, E. Wenzl i and R. Schiessel 1
1 University Clinic of Surgery I, Vienna General Hospital, Vienna, Austria
z Institute for Pathological Anatomy and Histology, University of Vienna, Austria
Abstract. The study was designed to select criteria

which influence the incidence of local recurrence
after radical anterior resection for rectal cancer.
Local recurrence developed in 18 patients (20%)
out of 90. All patients entered a prospective clinical
study for the detection of local recurrence (mean
observation time: 50 months). The following criteria were evaluated retrospectively: age, sex, staging, grading, gross appearance of the tumour, lymphatic reaction, invasion of lymph- and blood vessels, perineural invasion, mucus production of the
tumour and width of the distal margin of clearance
(measurement in cm in the specimen immediately
after resection). The incidence of local recurrence
(%) depended on Dukes stage (A: 7%, B: 17%,
C: 40%; p<0.03), grading (well differentiated:
5%, average: 20%, poorly differentiated: 55%;
p_< 0.02), gross appearance (protuberant: 15%, infiltrating: 47%; p <0.006), lymphatic stroma reaction (yes: 10%, no: 45%; p<0.006), invasion of
veins (yes: 75%, no: 20%; p<0.0002), perineural
invasion (yes: 52%, no: 17%; p<_0.001) and the
margin of clearance ( < 1 cm: 52%; 1 - 3 cm: 10%,
> 3 cm: 1 5 % ; p N 0 . 0 2 Mantel, p <0.05 Breslow between < 1 cm vs 1 - 3 cm and > 3 cm, respectively).
Local recurrence was not related to age, sex and
mucus production of the tumour. Unfavourable
morphological criteria may help to define groups
with a higher risk of developing local recurrence. A
tumour-free margin exceeding at least I cm appears
necessary to reduce the rate of local recurrence.
Low anterior resection with or without special

anastomotic techniques [1, 2] may well increase the
risk of local recurrence after rectal cancer, if applied injudiciously. The surgical aim of achieving
local radicality whilst preserving the sphincters
even in the presence of low rectal tumours prompts

a reconsideration of the rules and recommendations concerning a wide tumour-free distal margin
of resection. As local recurrence may also appear
after abdominoperineal excision the necessity for a
margin of clearance of at least 5 cm in anterior
resection has been questioned by several authors
[3-7]. Although in the individual case the risk of
recurrence may be anticipated on grounds of the
pathologist's report, the ultimate test of any method's oncological safety is in the recurrence rates of
major published series. We have therefore analysed
local recurrence after anterior resection for rectal
cancer with respect to those morphological criteria
which may have prognostic value.
Methods
Ninety out of 211 patients operated for rectal cancer between
January 1st 1977 and May 30th 1980 at our clinic underwent a
classical radical anterior resection with a handsutured transabdominal anastomosis. The patients (M: 43, F: 47; age: 66.4 9.8
years) were entered into a prospective follow-up study permitting analysis of local recurrences, which were defined as any
recurrent tumour growth within the pelvic field of surgery. Our
computer-aided follow-up programme scheduled patients for
regular examinations at intervals of three months during the
first two postoperative years, of six months from the year three
to five, and yearly intervals thereafter. Each follow-up examination comprised clinical check-up, blood chemistry (RBC, WBC,
liver function tests, CEA level) and sigmoidoscopy with inspection and, if necessary, biopsy of the anastomosis. Whenever
recurrent disease was suspected, investigations were carried further, including pulmonary X-ray, liver ultrasound and pelvic
CT.
A further two anterior resection patients were excluded
from the study since they developed true suture line recurrences
within the bowel lumen after local non-radical resection immediately at the distal edge of the tumour.
With the aim of detecting those factors that may increase
the risk of local recurrence, a number of criteria eleven variables altogether - were analysed retrospectively for all 90 pa-
196
tients. Those factors were: the patients' age and sex, the tumourfree margin of clearance as measured in centimetres by the
surgeon in the fresh specimen without tension, and the gross
appearance of the tumour, whether of protuberant or infiltrating type. All histological sections were re-examined by an unbiased pathologist: firstly, to check the tumour's stage according
to Dukes classification [8], and the grade according to the criteria of Dukes' and the WHO [9, 10]. Secondly, the sections of the
primary tumour were scrutinized for the presence or absence of
lymphatic stroma reaction, invasion of veins and lymphatic
vessels, perineural growth and mucus production.
Possible interdependence of the eleven criteria was investigated by the Chi-square-test applied to pairs of the variables in
contingency tables. The probability of remaining free of local
recurrence was estimated with Kaplan-Meier functions [11]. Statistical significance was calculated with the tests for censored
data of Breslow and Mantel with the level of significance defined
as p < 0.05. In order to define the prognostic importance of the
distal margin of clearance more precisely, this particular analysis was additionally stratified for the factors "staging" and
"grading" 9
100
8 patients
at risk
77.5
50
,(
ul
tO
o.
2
3
4
YEARS AFTER RADICAL A.R.
Fig. 1. Probability of remaining free of local recurrence after

radical anterior resection for rectal cancer (Kaplan-Meier estimation). Mean observation time: 50 months; local recurrence:
n=18
Results
100
The analysis of interdependence between pairs of

the eleven variables showed a significant relationship between the following factors.
1. Staging and grading: Well differentiated tumours were found in 50% of stage Dukes A, in
18% of stage Dukes B and in 4% of stage Dukes C.
An average differentiation was found in 50% of
Dukes A, 64% of Dukes B and 81% of Dukes C
patients. Poorly differentiated tumours were found
in 18% of stage Dukes B and 15% of stage Dukes
C; there were no poorly differentiated tumours in
stage Dukes A patients. (p_< 0.05, z2-test).
2. Staging and stroma reaction: lymphatic
stroma reaction was present in 77% of Dukes A,
62% of Dukes B and 30% of Dukes C tumours
(p < 0.004, )~2-test).
3. Type of growth and stroma reaction: lymphatic stroma reaction was present in 63% of the
protuberant, but only in 25% of the infiltrating
tumours (p < 0.003, xZ-test).
During a median observation interval of 50
months local recurrence appeared in 18 out of 90
patients (20%), mostly within the first two postoperative years. Sixty patients remained free of recurrence, six developed liver metastases, and six died
without evidence of disease.
The probability of remaining free of local recurrence was 80% after 3 years and 77.5% after six
years, with eight patients remaining at risk (Fig. 1).
During the entire period of observation the 75%
quartile was not reached.
Out of the eleven variables that were analysed
retrospectively, a significant prognostic influence
93
- -it
" ~ r -,
I
k . . . . . -'_ . . . . . . . . . . . . . . . . . . . . . . .
~j
-i
eo
OI
YEARS AFTER RADICAL A.R,

radical anterior resection for rectal cancer dependent of
"staging" (Kaplan-Meier estimation). - - Dukes A, n = 1 9 ;
. . . . Dukes B, n = 4 2 ; . . . . Dukes C, n = 2 9
was detected for all but three: there was no connection between the development of local recurrence
and the factors "age", "sex" and "mucus production". The local recurrence rate was significantly
influenced by staging (Fig. 2), grading (Fig. 3) and
the presence of perineural invasion (Fig. 4). Furthermore a local recurrence may be expected in
15 % of the patients with a distal margin of clearance of > 3 cm, in 10% with a margin of 1 - 3 cm
and in 52% with a margin of < 1 cm (Fig. 5). The
prognostic significance of the distal margin of
197
100
......
IO0
i _L..._
'__t
!
t
i
~_ . . . . . . . . . . . . . . . . . . . . . .
90
95
:'i
. . . . . . . . . . . . .
85
-i
i_._.
i
80
................
.i
i
i
i
i.
................
i
i
i
u.
48
uJ 4 5
2
YEARS AFTER
YEARS AFTER RADICAL A.R.

radical anterior resection for rectal cancer dependent on "grading" (Kaplan-Meier estimation). G I =well differentiated,
G 2 = average differentiation, G 3 = poorly differentiated.
--Gl,
n = 1 9 ; . . . . G2, n = 6 0 ; . . . . . G3, n = l l

radical anterior resection for rectal cancer dependent on the
"distal margin of clearance" (Kaplan-Meier estimation).
- - 1 - 3 cm, n = 32; . . . . > 3 cm, n = 4 0 ; . . . . . < 1 cm, n = 17
Table 1. Prognostic factors for the development of local recur-
100
'----89
rence after radical anterior resection for rectal cancer9 Observations differentiated for various levels. At the 75% quartile the
risk to develop local recurrence is 25%. The 75% quartile was
not reached in the observation time, when no value is given
I
*
83
RADICAL A,R.
L .....
i
L . . . . . . . . . . . . .
Variable
Levels
75%
quartile
reached
after: years
p values in
univariate
Breslow/
Mantel tests
Gross
appearance
Lymphatic
reaction
Invasion
of veins
Invasion of
lymph vessels
Perineural
invasion
protuberant
infiltrating
yes
no
yes
no
yes
no
yes
no
66
20
46
36
5
76
16
65
13
68
1.6
2.0
0.8
-1.2
1.3
-
p=0.015/
p = 0.006
p = 0.006 /
p = 0.003
p = 0.0002 /
p = 0.0004
p=0.005/
p=0.05
p =0.019/
p = 0.01
0g
u.
48
uJ
2
YEARS AFTER
3
RADICAL
A.R.

radical anterior resection for rectal cancer dependent on "perineural invasion" of the tumour (Kaplan-Meier estimation)9
- - No, n = 6 8 ; . . . . yes, n = 13
tion and, in the presence of venous or lymphatic

i n v a s i o n ( T a b l e 1).
clearance remained unaltered, when stratified and
analysed according to the variables "staging" and
"grading", which were distributed in similar prop o r t i o n s in all t h e t h r e e g r o u p s f o r d i s t a l m a r g i n .
The risk of developing local recurrence was also
significantly increased for infiltrating types of
g r o w t h , in t h e a b s e n c e o f a l y m p h a t i c s t r o m a r e a c -
Discussion
Sensible progress in surgical policy for rectal cancer
has always evolved from close cooperation between
surgeons and pathologists. Clearly, the argument
198
for the classical abdominoperineal excision [12] was
weakened when Westhues [13] and Dukes [14] had
demonstrated that the lymphatic spread of rectal
cancer was exclusively directed upwards along the
inferior mesenteric artery. These pathological findings suggested that preservation of the anal
sphincters should not increase the risk of local recurrence. In practice this concept was corroborated
by comparable local recurrence rates after radical
rectal excision and resection respectively [3, 6,
14-21]. Further research had and still has to concentrate on those factors that may give rise to local
recurrence despite an apparently radical operation.
Most of the 18 local recurrences developed
within the first two postoperative years, and this
justifies our initial frequency of follow-up examinations. Fourty-two percent of our patients who had
developed local recurrence could be reoperated
with the intention to cure [20].
Irrespective of any single factor's prognostic
value our analysis by pairs revealed that four of the
variables were significantly associated with each
other: turnouts with a high grade of differentiation
were less advanced in their stage and vice versa.
This finding is consistent with the relationship between staging and grading described by Dukes in
an analysis of 1000 cases [10], and implies that from
the pathological point of view our series is comparable with others [22]. Furthermore a lymphatic
stroma reaction was more often observed in early
tumour stages and in tumours with a protuberant
growth type. Tumours with a high grade of differentiation tend towards a less infiltrating growth,
often provoke a lymphatic reaction as a sign of
host-resistence and, therefore, are frequently at an
early stage. Low grade, early stage, protuberant
growth type and the presence of a lymphatic reaction by contrast were individually less often followed by a local recurrence.
In our patients the histological evidence of
venous, lymphatic, or perineural invasion around
the primary growth increases the risk of local recurrence. However, these factors were neither significantly associated with each other nor with turnout
grading or other qualities - which means that each
of them may obscure the prognosis even in the
presence of a carcinoma with otherwise less harmful morphological characteristics. The presence of
perineural invasion, for instance, may explain pelvic recurrence after resection of even a Dukes A
tumour.
Considering that a single unfavourable histological feature may contribute to local recurrence, it is
not surprising that the incidence after any type of
surgery for rectal cancer has remained virtually un-
changed over the last decades. At our clinic the local

recurrence rates are 14% after anterior resection
and 17% after abdominoperineal excision [20, 23].
In the literature these rates average around 20% [3,
17, 24], with a range from 15 to 50% [4, 16, 25].
The importance of individual prognostic factors in different reports is difficult to assess. There
is often disagreement between authors, and evaluation is based either on the percentage incidence of
local recurrences or on 5-year survival rates that
also depend on cases which may be free of local
recurrence but which have distant metastases.
There was no difference in local recurrence rates
between anterior resection and abdominoperineal
excision in the series of Hermanek (23%) [17] and
Slanetz (24%) [26], whereas Phillips and coworkers
observed significantly more local recurrence following anterior resection (18%) than following abdominoperineal excision (12%) [27, 28]. In an analysis of a total of 2948 cases from the St. Mark's
Hospital Lockhart-Mummery found a 5-year survival rate of 67% after anterior resection and of
53% after abdominoperineal excision, the difference being explained by a preponderance of highly
differentiated tumours of stages Dukes A and B in
the group of sphincter-saving resections [29]. A
subsequent analysis by Nicholls and coworkers did
not show a difference in survival rates between the
two operative methods [30].
With respect to staging and grading our results
are in keeping with those of Morson [3] and
Hermanek [16-18]. However, according to Phillips
[27, 28] only staging has prognostic importance,
whereas Malmberg [21] could not find any influence from either factor. As far as other tumour
characteristics are concerned, the significance of
carcinoma type, nodal involvement and mucus production was described by Hermanek [16-18] and
the influence of venous invasion by Talbot [31].
Once the preservation of the anal sphincters
without oncological risk was possible, the classical
anterior resection [32] for high rectal tumours was
followed by special sphincter-saving operations,
such as transsphincteric [33] or abdominosacral
[15] procedures, coloanal anastomosis [1] and the
use of the stapler [2]. Although each of these methods is meant to extend the scope of resection and
restoration of continuity distally beyond the level
of "mid-third" rectal cancer, their application is
often limited if one adheres strictly to the rule of a
margin of clearance of 5 cm to the tumour. Since
some extreme sphincter-saving procedures - coloanal anastomosis and stapling in particular have become a widespread technical routine, the
extent of the "safety-margin" is being continuously
199
reappraised. Originally, the necessity for a wide

margin of clearance has been claimed on grounds
of anecdotal reports of microscopical distal intramural spread of several centimetres [34, 35]. This is,
however, an extremely rare finding, only encountered in cases too far advanced for radical cure
anyway. Therefore it appears unjustified to observe
a margin of 5 cm for example, as this will often
mean unnecessary sacrifice of the anal sphincters.
Goligher [14] found distal intramural spread in
only 2% of his patients, whereas Williams and coworkers [7] in an analysis of 50 consecutive cases
observed distal spread in 24%. The spread reached
beyond 1 cm in 10% of the specimens, always in
connection with an advanced tumour of low grade.
With serial sections Heald [36] demonstrated extramural distal cancer spread and consequently advocated thorough removal of the mesorectum beyond
the line of resection.
Obviously, the incidence and extent of distal
tumour spread varies between authors, which may
partly be due to different methods of measuring the
tumour-free margin. Originally, Hermanek and
Gall [25] maintained a safety margin of 5 cm in the
mobilized rectum which in the freshly resected
specimen is equally 5 cm, if measured with tension,
and corresponds to 3 cm if measured without tension. Due to tissue shrinkage measurements in a
fixed specimen (with or without previous tension)
may result in deceivingly shorter margins of clearance [6, 7, 37] than if assessed before fixation [4, 16,
17, 25]. The margin of clearance in our specimens
was measured immediately after the resection,
without tension. This enables the surgeon to resect
subsequently an additional cuff from the rectal
stump, should the original margin of clearance
prove shorter than expected or even contain tumour cells in frozen section.
There appears to be growing agreement for a
tumour-free margin of less than 5 cm as oncologically safe, except in the presence of a highly malignant tumour. According to Goligher a margin of
clearance of 2.5 to 3 cm is sufficient and may even
be reduced to 1.5 to 2 cm in highly differentiated
tumours of a protuberant growth type [37]. Similarly, Hermanek will now tolerate less than his otherwise strict limit of 3 cm in cases of high grade
Dukes A tumours [4, 16, 17]. A tumour-free margin
(fixed tissue) of 1 to 2.5 cm is advocated by Williams [7], 2 cm by Heald [36] and up to 3 cm by
Pollett and coauthors [5, 6]. The safety of these
recommendations is confirmed by our own results.
Therefore it seems that the risk of a local recurrence after radical anterior resection is significantly
increased for both, morphological and technical
reasons, naturally independent of each other. Firstly, unfavourable morphological tumour characteristics may predispose to pelvic recurrent disease
despite a wide tumour-free margin. Secondly, a
narrow zone of clearance may jeopardize a definitive cure even in tumours with otherwise excellent
prognostic qualities. Technical causes must certainly also include insufficient excision of perirectal fat
[7, 36]. Theoretically intraoperative spillage of viable tumour cells may be of importance [3, 26], although the role of cancer cell implantation at the
suture line remains unclear [38].
This study and similar reports may have implications for rectal cancer surgery policy. Preoperative assessment should take into account unfavourable tumour characteristics, such as infiltrating growth type in sigmoidoscopy and low grade of
differentiation in biopsies. Accordingly, a protuberant growth type and high grade of differentiation
found preoperatively, without macroscopical evidence of lymphatic spread during the operation,
may allow the choice of a less extensive margin of
clearance and, therefore, help to preserve continence even in low rectal cancer. For such a tumour
type we accept a tumour-free margin of resection of
2 to 3 cm. However, it is doubtful whether patients
with a highly malignant tumour, in particular with
perineural invasion, will actually benefit from a
wide margin of resection at all. Despite the oncological safety of a margin of 1 to 3 cm in our series we
still believe it unwise to use radical resections closer
than 2 cm beyond the inferior tumour edge, unless
a patient refuses to live with a permanent stoma.
Complete removal of the perirectal fat, exposing
the pelvic floor, should become surgical routine,
even in tumours of the middle rectal third.
The final pathological report, evaluating every
factor of prognostic relevance prompts definition
of "high-risk" groups of patients who, at follow-up
examination, which should include pelvic CT at
regular intervals, must be scrutinized for signs of
local recurrence, particularly during the first two
postoperative years. Furthermore, the possibility of
adjuvant cancer therapy, local radiotherapy in particular, within controlled trials, should in the first
place be offered to patients with a significantly
higher adverse prognostic risk.
References
1. Parks AG, Percy JP (1982) Resection and sutured colo-anal
anastomosis for rectal carcinoma. Br J Surg 69:301-304
2. Heald RJ (1980) Towards fewer colostomies: the impact of
circular stapling devices on the surgery of rectal cancer in a
district hospital. Br J Surg 67:198-200
200
3. Morson BC, Vaughan EG, Bussey HJR (1963) Pelvic recurrence after excision of the rectum for carcinoma. Br Med J
2:13-18
4. Hermanek P, Gall FP (1981) Der aborale Sicherheitsabstand bei der sphinktererhaltenden Rektumresektion.
Chirurg 52:25 29
5. Pollett WJ, Nicholls RJ (1981) Does the extent of distal
clearance affect survival after radical anterior resection for
carcinoma of the rectum? G U T 22:872
6. Pollett WG, Nicholls RJ (1983) The relationship between
the extent of distal clearance and survival and local recurrence rates after curative anterior resection for carcinoma of
the rectum. Ann Surg 198:159-163
7. Williams NS, Dixon MF, Johnston D (1983) Reappraisal of
the 5 centimeters rule of distal excision for carcinoma of the
rectum: a study of distal intramural spread and of patients'
survival. Br J Surg 70:150-154
8. Dukes CE (1932) The classification of cancer of the rectum.
J Pathol Bacteriol 35:323-330
9. Dukes CE (1936) Histological grading of rectal cancer. Proc
R Soc Med 30:371-376
10. Dukes CE (1940) Cancer of the rectum: an analysis of 1000
cases. J Pathol 50:527-535
11. Kaplan EL, Meier P (1958) Nonparametric estimation from
incomplete observations. Am Statist Assoc 53:457 481
12. Miles WE (1908) A method of performing abdominoperineal excision for carcinomas of the rectum and the terminal portion of the pelvic colon. Lancet 2:1812-1816
13. Westhues H (1930) Ober die Entstehung und Vermeidung
des lokalen Rektumkarzinom-Rezidivs. Arch Klin Chir
161:582-624
14. Goligher JC, Dukes CE, Bussey HJR (1951) Local recurrence after sphincter-saving excisions for carcinoma of the
rectum and rectosigmoid. Br J Surg 39:199-211
15. Localio SA, Eng K, Gouge TH, Ranson JHC (1978) Abdominosacral resection for carcinoma of the midrectum: ten
years experience. Ann Surg 188:475-480
16. Hermanek P, Gunselmann W, Altendorf A, Gall FP, Horbach L (1981) Vorhersage von Lokalrezidiven nach Operationen von Karzinomen des mittleren Rektumdrittels.
Langenbecks Arch Chir 354:133-146
17. Hermanek P, Gall FP, Altendorf A (1981) Lokalrezidive
nach Rektumkarzinom Entstehung, Diagnose, Prognose.
Langenbecks Arch Chir 356:289-298
18. Schiessel R, Wunderlich M, Kovats E, Rauhs R (1983) Die
Therapie des Lokalrezidivs nach kolorektalem Karzinom.
Wi Kli Wochenschr 9 5 : 2 - 4
19. Adloff M, Arnaud JP, Schloegel M, Thibaud D (1985) Factors influencing local recurrence after abdominoperineal
resection for cancer of the rectum. Dis Col Rect 28:413 415
20. Schiessel R, Wunderlich M, Herbst F (1986) Local recurrence of colorectal cancer: effect of early detection and aggressive surgery. Br J Surg 73:342 344
21. Malmberg M, Graffner H, Ling L, Olsson SA (1986) Recurrence and survival after anterior resection of the rectum
using the end to end anastomotic stapler. Surg Gynecol
Obstet 163:231-234
22. Freedman LS, Macaskill P, Smith AN (1984) Multivariate
analysis of prognostic factors for operable rectal cancer.
Lancet 2:733-736
23. Wenzl E, Wunderlich M, Herbst F, Schemper M, Fell W,

Rauhs R, Schiessel R (1986) Konsequenzen der Nachsorge
beim kolorektalen Karzinom. Wi Kli Wochenschr
98:851-855
24. Schiessel R, Wunderlich M, Kovats E, Rauhs R (1983)
Sphinktererhaltung beim Rektumkarzinom: M6glichkeiten
und Grenzen der vorderen Resektion. Wi Kli Wochenschr
95:769-773
25. Gall FP, Hermanek P (1981) Kontinenzerhaltende Operationen beim Rektumkarzinom. Langenbecks Arch Chir
354:45-53
26. Slanetz CA, Herter FP, Grinnell RS (1972) Anterior resection versus abdominoperineal resection for cancer of the
rectum and rectosigmoid. Am J Surg 123:110-117
27. Phillips RKS, Hittinger R, Blesovsky L, Fry JS, Fielding LP
(1984) Local recurrence following "curative" surgery for
large bowel cancer: I. The overall picture. Br J Surg
71:12-16
28. Phillips RKS, Hittinger R, Blesovsky L, Fry JS, Fielding LP
(1984) Local recurrence following "curative" surgery for
large bowel cancer: II. The rectum and the rectosigmoid. Br
J Surg 71:17 20
29. Lockhart-Mummery HE, Ritchie JK, Hawley PR (1976)
The results of surgical treatment for carcinoma of the rectum at St. Mark's Hospital from 1948 to 1972. Br J Surg
63:673-677
30. Nicholls RJ, Ritchie JK, Wadsworth J, Parks AG (1979)
Total excision or restorative resection for carcinoma of the
middle third of the rectum. Br J Surg 66:625-627
31. Talbot IC, Ritchie J, Leighton MH, Hughes AO, Bussey
H JR, Morson BC (1980) The clinical significance of invasion of veins by rectal cancer. Br J Surg 67:439-442
32. Dixon CF (1948) Anterior resection for malignant lesions of
the upper part of the rectum and the lower part of the
sigmoid. Ann Surg 128:425-442
33. Mason AY (1970) Surgical access to the rectum - a transsphincteric approach. Proc R Soc Med [Suppl] 63:91-94
34. Quer EA, Dahlin DC, Mayo CW (1953) Retrograde intramural spread of carcinoma of the rectum and rectosigmoid.
Surg Gynecol Obstet 96:24-30
35. Grinnell RS (1954) Distal intramural spread of carcinoma
of the rectum and rectosigmoid. Surg Gynecol Obstet
99:421 430
36. Heald RJ, Husband EM, Ryall R D H (1982) The mesorectum in rectal cancer surgery - the clue to pelvic recurrence?
Br J Surg 69:613-616
37. Goligher J (1984) Surgery of the anus, rectum and colon.
5th edn. Bailliere Tindall, London, p 441
38. Goligher J (1984) Surgery of the anus, rectum and colon.
5th edn. Bailliere Tindall, London, p 756
Dr. Wolfgang Fell
I. Chirurgische Universit/itsklinik
Allgemeines Krankenhaus
Alser Strasse 4
A-1090 Wien
Austria
Col6i'eeial
Disease
Gastric carcinoma and familial adenomatous polyposis (FAP)

A.J. Goodman i, S . A . C . Dundas 2, j . H . Scholefield i and B.F. Johnson 1
Department of 1 Surgery and 2 Pathology, Royal Hallamshire Hospital, Sheffield, U K
Abstract. We report two cases of FAP associated

with gastric carcinoma. The literature on this subject, with special reference to 'fundic gland polyposis' is reviewed.
A familial type of multiple colonic adenomatous

polyposis was first described by Cripps in 1882 [1].
Until recently these adenomatous polyps were
thought to be 'confined to the large intestine' [2].
This set FAP apart from the other inherited polyposis syndromes, Peutz-Jeghers and juvenile polyposis, where the whole gastrointestinal tract can be
involved. However, as early as 1895 Hauser reported an association between FAP and multiple
gastric polyps [3]. The Japanese showed that most
patients with FAP had adenomas elsewhere; close
to 100% in the duodenum and 50% in the gastric
antrum [4]. However, these figures are not supported by Western experience where duodenal
adenomas were present in 33% of cases and gastric
adenomas found in only 2% of patients with FAP
[5]. It is possible that the higher incidence of gastric
carcinoma in the general population in Japan has
led to this over-emphasis of the risk of gastric adenomas and cancer in polyposis patients in Japan. It
is now known that the duodenal adenomas, like
those in the colon, undergo the adenoma-carcinoma sequence, making periampullary carcinoma
the commonest extra-colonic site of malignancy in
FAP [4]. Murphy, in 1962, was the first to describe
concomitant gastric carcinoma in FAP, arising
from an antral adenoma [6]. In 1977, Watanabe et
al. reported a further three cases and reviewed the
world literature of seven cases; of these ten, eight
were reported from Japan [4]. In the same paper
they reported multiple hamartomatous polyps in
the body and fundus of the stomach in six patients
of 26 studied with FAP. They termed these polyps

'fundic gland polyposis' and stated they were
unique to FAP.
We report a further two cases of FAP associated
with gastric carcinoma and 'fundic gland polyposis'.
Case 1
A 50 year old lady was diagnosed as suffering from FAP in 1971
(age 33). Rectal biopsies showed multiple adenomatous polyps
with no evidence of malignancy. Her brother and father had
both died of colonic carcinoma aged less than 40 years. She
underwent colectomy with ileo-rectal anastomosis in 1971; the
resected specimen showed no areas of malignant change. She
remained well until October 1986, when she noticed constant
epigastric pain, which radiated through to her back and was
relieved by antacids. Physical examination revealed epigastric
tenderness only. Gastroscopy showed numerous small polyps
Fig. 1. There is a partially ulcerated fungating tumour in the

mid-part of the hemigastrectomy specimen. The surrounding
mucosa shows hundreds of 'fundic polyps'
202
Fig. 2. Hyperplastic 'fundic gland

polyp' of body mucosa (original
magnification x I0)
Fig. 3. A Fundic gland polyp showing adenomatous dysplasia (boxed

area) (original magnification x 10).
B High power view of boxed area
showing irregular glands lined by
tall epithelium with hyperchromatic nuclei (original magnification
x 40)
throughout the fundus and body of stomach, with a large
fungating polypoid carcinoma with central ulceration on the
greater curve. The antrum was spared, the mucosa looking entirely normal, as did the pylorus and duodenum. Surprisingly,
endoscopic biopsies of the main lesion showed fundic gland
polyps, initially reported as hyperplastic polyps, without dysplastic change.
Before laparotomy, a small bowel enema and liver ultrasound were reported as normal.
At laparotomy, there was a large carcinoma of the upper
body of the stomach (Fig. 1) directly infiltrating the spleen; the
left ovary was enlarged, and histology showed metastatic gastric
adenocarcinoma. A palliative hemigastrectomy, splenectomy
and left oophorectomy were carried out. Microscopy showed
the main tumour to be a moderately differentiated adenocarcinoma of intestinal type. Most of the remaining polyps were
composed of hyperplastic focally cystic fundic glands of the type
termed 'fundic gland polyps' by Watanabe et al. (Fig. 2). Many

of these showed surface epithelial hyperplasia. Some polyps
displayed adenomatous dysplasia with intramucosal proliferation of irregular glands lined by tall epithelium with hyperchromatic nuclei (Fig. 3). Since these dysplastic areas were histologically identical to the carcinoma of the luminal surface, it is
highly probable that the adenomatous change was a precursor
to the carcinoma. Furthermore, other fundie gland polyps adjacent to the carcinoma contained focal intramucosal carcinoma
which, by serial sectioning, could be shown to be discontinuous
with the carcinoma.
Case 2
A 63 year old man diagnosed as having FAP in 1951, was treated
that year with a pan-proctocolectomy and ileostomy. His father
203
and brother had died of colonic carcinoma before the age of 40
years. He remained well until November 1984 (33 years) when
he noticed epigastric pain before and after food. An oral cholecystogram showed multiple gallstones, and he was referred for
surgery due to continuing pain. Laparotomy showed a thickwalled gallbladder (not containing stones) which was adherent
to a large active duodenal ulcer (DU). This was treated by highly
selective vagotomy. After initial relief his pain returned, and
gastroscopy revealed a large DU covered in slough. He was
readmitted for further surgery and noted to have three polyps on
his spout ileostomy.
Laparotomy showed a large DU penetrating the gallbladder; the gastric antrum was thickened and contracted. A
Polya partial gastrectomy and cholecystectomy were performed.
Several polyps were removed from the duodenum, as was a
further one from the mid-jejunum.
Microscopy of the resected specimens revealed a well differentiated adenocarcinoma of the gastric antrum, and fundic
gland polyps similar to those in Case 1. The duodenal, jejunal
and ileostomy polyps were all tubulo-villous adenomas.
carcinoma. The presence of the polyps increases the

number of epithelial cells exposed to carcinogenic
agents; therefore an increased incidence of adenomatous change and carcinoma would be expected,
as has recently been recognised with hamartomatous polyps in Peutz-Jeghers syndrome and
juvenile polyposis [10].
In Case 1 we have strong histological evidence
that adenomatous dysplasia in the fundic gland
polyps was a precursor of the carcinoma. This new
evidence, plus the known malignant potential of
gastric and duodenal adenomata, supports the argument for regular endoscopic surveillance of the
upper gastrointestinal tract in patients with FAP.
References
Discussion
Although the association between FAP and extracolonic tumour has been recognised for over 90
years, the frequency of gastric polyps in FAP is not
widely appreciated by clinicians. Most series are
from Japan, and report various gastric lesions to be
present in 55-67% of patients with FAP [4, 7, 8];
gastric adenomata are the commonest, usually arising in the antrum. Watanabe first recognised
'fundic gland polyposis' to be a distinct histological
entity, thought to be unique to FAP. Fundic gland
polyposis occurs in approximately one third of patients with FAP. However, it does occur rarely in
non-FAP patients; the incidence in Japan is 0.085%
[9]. Fundic gland polyps have been confused with
the much commoner hyperplastic or regenerative
polyposis, as occurred initially in Case 1. In contrast to hyperplastic polyps, fundic gland polyps
are smaller, occur throughout the fundus and body
rather than at the junction of body and antrum,
have shallower pits and the stroma does not contain smooth muscle or collagen. They have been
classed as hamartomas; however, when these occur
in the gastrointestinal tract they are predominantly
composed of connective tissue elements. Fundic
gland polyps are almost entirely composed of epithelial elements, and we are therefore circumspect
about their origin. Unlike gastric adenomas, fundic
gland polyps have not previously been considered
as pre-malignant. In both the reported cases, no
gastric adenomas were present, but adenocarcinoma arose within mucosa studded with fundic
gland polyps. In Case 1, adenomatous change and
intramucosal carcinoma was identified in fundic
gland polyps discontinuous with the main gastric
1. Cripps HW (1882) Two cases of disseminated polyps of the

rectum. Trans Pathol Soc Lond 33:165-168
2. Bussey HJR (1975) Familial polyposis coli. Johns Hopkins
University Press, Baltimore London
3. Hauser G (1895) Ober Polyposis intestinalis adenomatosa
und deren Beziehungen zur Krebsentwicklung. Arch F Klin
Med 55:429-448
4. Watanabe H, Enjoji M, Yao T, Iida M, Ohsato K (1977)
Accompanying gastro-enteric lesions in familial adenomatosis coli. Acta Pathol Jpn 27:823-839
5. Sarre RG, Frost AG, Jagelman DG, Petras RE, Sivak MV,
McGannon E (1987) Gastric and duodenal polyps in familial adenomatous polyposis: a prospective study of the nature and prevalence of upper gastrointestinal polyps. Gut
28:306 314
6. Murphy ES, Mireless MV, Beltran AO (1962) Familial
polyposis of the colon and gastric carcinoma. Concurrent
conditions in a 16 year old boy. JAMA 179 1026-1028
7. Ushio K, Okazaki M, Takasugi T, Hagiwara K, Matsue H,
Sasagawa M, Doi I, Yamada T, Ichikawa H (1974) Lesions
associated with the so-called familial polyposis of the colon.
Stomach and Intestine 9:1137-1148
8. Ohsato K, Itoh H, Ikea S, Nishimura M, Yao T, Iida M,
Watanabe H (1974) Follow-up study on upper gastrointestinal lesions in familial polyposis of the colon. Jpn J
Gastroenterol 72:141 - 148
9. Iida M, Yao T, Watanabe H, Itoh H, Iwashita A (1984)
Fundic gland polyposis in patients without familial adenomatosis coli: its incidence and clinical features. Gastroenterology 86:1437-1442
10. Bussey HJR (1984) Gastrointestinal polyposis syndromes.
In: Antony PP, MacSween RNM (eds) Recent advances in
histopathology, 12. Churchill Livingstone, Edinburgh,
pp 169-177
Accepted: 23 May 1988
Mr. A. J. Goodman
University Surgical Unit
Floor K
Royal Hallamshire Hospital
Sheffield S10 2JF
UK
Colo 'eeial
Disease
Int J Colorect Dis (1988) 3 : 2 0 4 - 2 0 6
Intraoperative irrigation and primary resection for obstructing lesions

of the left colon
F. Konishi 1, T. M u t o
2,
K. K a n a z a w a 1 and Y. M o r i o k a 2
1 Department of Surgery, Jichi Medical School and 2 The First Department of Surgery, University of Tokyo, Tokyo, Japan
Abstract. The treatment of choice for left sided

colonic obstruction is still controversial. We tried
primary resection and anastomosis with the aid of
intraoperative irrigation of the dilated proximal colon. Twenty-one cases of obstructive carcinoma of
the left colon and four cases of sigmoid colon volvulus were managed using this approach. After the
antegrade or retrograde intraoperative irrigation,
primary resection and anastomosis without colostomy was performed in all 25 cases. There was only
one case with anastomotic leakage. The satisfactory results of our present study and of the previous reports of intraoperative irrigation lead us to
recommend intraoperative irrigation and primary
anastomosis for left sided colonic obstruction except when the general condition of a patient is very
poor or when the prognosis is expected to be poor
due to the advanced spread of carcinoma.
The surgical treatment of obstructive lesions of the

left colon remains controversial. Anastomosis of
the faecally loaded colon has been associated with
a high incidence of anastomotic breakdown [1-6].
Two stage or three stage operations have been advocated and are in widespread use. However such
procedures necessitate a long hospital stay and patients have to endure more surgery. The morbidity
and mortality of performing more than two operations in patients with colonic carcinoma, who are
often over 60 years old, are high [7-9]. We report
our experience of primary resection and anastomosis for left sided colonic obstruction, carried out
using intraoperative bowel irrigation and employing a tube which we designed for this purpose.
Patients and methods

From 1981 to 1986, 25 patients with obstruction of the left colon
underwent primary resection and anastomosis with intraoperative bowel irrigation in one of the two medical schools and the
two affiliated hospitals. There were 21 cases of colorectal carcin o m a and 4 cases of sigmoid colon volvulus without ischaemic
necrosis. The age and sex of these patients, and site of the lesions
are shown in Table 1.
Our irrigation tube was designed according to the original
idea of Muir which was reported in 1968 [10]. The tube consists
of the hard tube and connecting soft flexible tubes. In the middle
of the hard part, a small side tube is attached. There are two
ring-like flanges at one end of this hard part of the irrigation
tube (Fig. 1). These flanges are used to fix the tube securely
within the bowel. At the other end of the hard part of the tube,
a flexible tube for drainage of the bowel contents is attached. A
small flexible tube, which is attached to the side tube, is connected to a container so that saline for irrigation can be introduced into the bowel lumen (Fig. 2).
After sufficiently mobilising the colon, accumulated bowel
contents proximal to the tumour were pushed back towards the
proximal part and a bowel clamp was laid approximately 10 cm
proximal to the tumour. A purse-string suture was placed between the tumour and the bowel clamp. The bowel wall was
incised in the middle of the purse-string suture and the hard part
of the irrigation tube with flanges was inserted into the bowel
lumen. A thick silk thread was laid around the bowel and tied
tightly over the tube in between the two flanges so that the tube
would not be detached. In the cases of sigmoid colon volvulus,
Table 1. Patients subjected to intraoperative irrigation and primary resection (25 cases)
Carcinoma of the left colon, 21 cases

Age 4 2 - 8 4 year old (Mean 61.1)
Male 13, Female 8
Site
Splenic flexure
Descending colon
Sigmoid colon
Recto-sigmoid
Rectum
Volvulus of the sigmoid colon, 4 cases
Age 3 0 - 7 0 year old (mean 50.3)
Male 4, female 0
205
In cases of both obstructing carcinoma and sigmoid colon
volvulus, the irrigation was followed by resection of the colon
and primary anastomosis end-to-end, or side-to-end if there was
disparity of size in the ends of the colon to be anastomosed.
Stapled anastomosis was performed in 6 cases and hand suture
anastomosis in 19 cases. Defunctioning eolostomy or tube caecostomy was not constructed.
Results
Fig. 1. Irrigation tube. Note the two flange like structures which
are used to fix the tube securely in the lumen of the colon
after reduction of the volvulus, the irrigation tube was inserted

into the sigmoid colon in the same fashion as in the obstructive
carcinoma cases.
The retrograde irrigation was performed as follows. Approximately 500 ml of saline was infused through the side tube
while clamping the draining tube, and the diluted bowel contents were evacuated through the draining tube (Fig. 2). This
procedure was repeated until the drained bowel contents became
clear. In the antegrade irrigation, a small catheter was inserted
through the appendix when an appendicectomy had not been
done, or alternatively the catheter was inserted through a small
incision of the terminal ileum. Saline was continuously infused
through the catheter into the right colon. The faeces in the
obstructed bowel were washed out through the draining tube
which was inserted immediately proximal to the tumour (Fig. 3).
In the antegrade irrigation, when there were impacted formed
faeces, retrograde irrigation through the side tube was also performed to facilitate the evacuation of the solid faeces in the left
colon. The catheter inserted through the ileum or the appendix
was removed after completion of the bowel irrigation. In both
retrograde and antegrade irrigation, manual compression of the
colon was necessary to facilitate the evacuation of the bowel
contents which were diluted with the infused saline.
The time taken for intraoperative irrigation was

about 1 h when the trial started, reducing to about
30 m i n w i t h m o r e e x p e r i e n c e . T h e v o l u m e o f s a l i n e
u s e d f o r i r r i g a t i o n r a n g e d f r o m 2 - 1 9 1. W e t r i e d
both retrograde and antegrade irrigation and
f o u n d t h a t a n t e g r a d e w a s m o r e effective. I n s e v e r a l
cases there was minor soiling of the peritoneal cavity w i t h faeces d u r i n g i n s e r t i o n a n d r e m o v a l o f t h e
irrigation tube, but this did not lead to any major
septic postoperative complications. Anastomotic
l e a k a g e o c c u r r e d in o n l y o n e p a t i e n t , a g e n e r a l l y
debilitated individual with advanced lung cancer.
The patient subsequently died. Routine postoperative c o n t r a s t s t u d i e s w e r e n o t p e r f o r m e d . A p a r t
from one patient who suffered postoperative intestinal obstruction requiring reoperation, there were
no other major postoperative complications.
Discussion
T h e first a t t e m p t a t o n e s t a g e o p e r a t i o n f o r left
sided colonic anastomosis using intraoperative
b o w e l i r r i g a t i o n w a s r e p o r t e d b y M u i r in 1968 [10].
yTu
Fig. 2. Retrograde irrigation
Fig. 3. Antegrade irrigation
206
Table 2. The rate of anastomotic leakage in the previous reports
Acknowledgements. The authors would like to thank Dr. T.
and in the present study of intraoperative irrigation
Yamamoto and Dr. H. Shida at Tokyo Koseinenkin Hospital

and Dr. Y. Kobayashi at Kanto Rosai Hospital for their cooperation.
Leakage rate
Radcliffe et al. (1983)
Koruth et al. (/985)
Pollock et al. (1987)
Present study
2/6/
4/47
4/41
(minor leakage)
1/25
H e used a specially designed irrigation tube which

we a d o p t e d w h e n we designed o u r own. In his rep o r t eight cases with left sided colonic o b s t r u c t i o n
were subjected to this procedure. H o w e v e r the
n u m b e r o f cases with p o s t o p e r a t i v e c o m p l i c a t i o n s
such as a n a s t o m o t i c leakage was not stated in the
report. In 1980 [11] a n d 1983 [12] D u d l e y a n d R a d cliffe r e p o r t e d their results with i n t r a o p e r a t i v e irrigation a n d p r i m a r y a n a s t o m o s i s . In their r e p o r t o f
1983 they experienced a n a s t o m o t i c leakage in 2 out
o f 64 cases. M o r e recently there were two o t h e r
reports o f i n t r a o p e r a t i v e irrigation a n d p r i m a r y
a n a s t o m o s i s for left sided colonic o b s t r u c t i o n [13,
14]. T h e leakage rates in the three previous reports
and in o u r study are s h o w n in Table 2. In a n o t h e r
r e p o r t by T h o m s o n [15] it is difficult to evaluate the
leakage rate as n o n - o b s t r u c t i n g rectal c a r c i n o m a s
a n d left sided colonic o b s t r u c t i o n cases were t a b u lated together. In o u r series we experienced only
one case o f a n a s t o m o t i c leakage. Before the introd u c t i o n o f the o p e r a t i v e irrigation, we p e r f o r m e d
various p r o c e d u r e s in 47 cases with left sided colonic o b s t r u c t i o n including two or three stage resections, H a r t m a n n ' s o p e r a t i o n , Paul-Mikulicz operation, Miles's o p e r a t i o n , a n d p r i m a r y resection with
a n a s t o m o s i s . T h e rate o f a n a s t o m o t i c leakage in
the 12 cases o f p r i m a r y resection with a n a s t o m o s i s
was 30%. F o s t e r et al. [16] r e p o r t e d an experimental s t u d y o f i n t r a o p e r a t i v e irrigation a n d p r i m a r y
resection in a rat m o d e l o f distal colonic obstruction. T h e y showed t h a t the a n a s t o m o t i c collagen
content was greater in the irrigated g r o u p t h a n in
the n o n - i r r i g a t e d group.
It takes a p p r o x i m a t e l y 30 m i n to do the intraoperative irrigation, which is an acceptable time
even in such an urgent o p e r a t i o n . In o r d e r to perf o r m the p r o c e d u r e s m o o t h l y a n d safely w i t h o u t
spillage o f faeces, it is i m p o r t a n t to h a v e a s t a f f
surgeon with g o o d experience o f the p r o c e d u r e in
the o p e r a t i n g team. With o u r results we will continue to p e r f o r m the i n t r a o p e r a t i v e irrigation a n d prim a r y a n a s t o m o s i s for left sided colonic o b s t r u c t i o n
except w h e n the general condition o f the patient is
very p o o r or w h e n the prognosis is p o o r due to
extensive s p r e a d o f c a r c i n o m a .
References
1. Irvin TT, Goligher JC (1973) Aetiology of disruption of

intestinal anastomoses. Br J Surg 60:461-464
2. Irvin TT, Greaney MG (1977) The treatment of colonic
cancer presenting with intestinal obstruction. Br J Surg
64:741-744
3. Smith SRG, Connolly JC, Gilmore OJA (1983) The effect of
faecal loading on colonic anastomotic healing. Br J Surg
70:49-50
4. Atik M, Castleberry JW, Werner JC, Cohn I (1960) An
experimental study of primary anastomosis of the obstructed colon. Surg Gynecol Obstet 109:697 701
5. White CM, Macfie J (1985) Immediate colectomy and primary anastomosis for acute obstruction due to carcinoma of
the left colon and rectum. Dis Colon Rectum 28:155-157
6. Welch JP, Donaldson GA (1974) Management of severe
obstruction of the large bowel due to malignant disease. Am
J Surg 127:492 499
7. Clark J, Hall AW, Moossa AR (1975) Treatment of obstructing cancer of the colon and rectum. Surg Gynecol
Obstet 141:541'-544
8. Carson SN, Poticha SM, Shields TW (1977) Carcinoma
obstructing the left side of the colon. Arch Surg
112:523-526
9. Phillips RKS, Hittinger R, Fry JS, Fielding LP (1985) Malignant large bowel obstruction. Br J Surg 72:296-302
10. Muir EG (1968) Safety in colonic resection. Proc R Soc Med
61:401-408
11. Dudley HAF, Radcliffe AG, McGeehan D (1980) Intraoperative irrigation of the colon to permit primary anastomosis. Br J Surg 67:80-81
12. Radcliffe AG, Dudley HAF (1983) Intraoperative antegrade irrigation on the large intestine. Surg Gynecol Obstet
156:721 --723
13. Koruth NM, Krukowski ZH, Youngson GG, Hendry WS,
Logie JRC, Jones RF, Munro A (1985) Intra-operative colonic irrigation in the management of left-sided large bowel
emergencies. Br J Surg 72:708-711
14. Pollock AV, Playforth MJ, Evans M (1987) Peroperative
lavage of the obstructed left colon to allow safe primary
anastomosis. Dis Colon Rectum 30:171-173
15. Thomson WHF, Carter SStC (1986) On-table lavage to
achieve safe restorative rectal and emergency left colonic
resection without covering colostomy. Br J Surg 73:61-63
16. Foster ME, Johnson CD, Billings P J, Davies PW, Leaper
DJ (1986) Intraoperative antegrade lavage and anastomotic
healing in acute colonic obstruction. Dis Colon Rectum
29:255-259
Dr. Fumio Konishi
Department of Surgery
Jichi Medical School
3311-1 Yakushiji Minamikawachimachi
Kawachigun, Tochigiken
329-04 Japan
Colo~
Disease
Function of the striated anal sphincter during straining

in control subjects and constipated patients
with a radiologically normal rectum or idiopathic megacolon
P . R . H . Barnes and J.E. Lennard-Jones
st. Mark's Hospital, London, UK
Abstract. T h e function o f the striated anal sphincter during d e f a e c a t i o n straining was r e c o r d e d by

m a n o m e t r y and e l e c t r o m y o g r a p h y ( E . M . G . ) in 31
c o n s t i p a t e d patients w h o were u n a b l e to expel a
water-filled rectal b a l l o o n with effort. This g r o u p
was divided on the basis o f m e a s u r e m e n t o f colonic
d i a m e t e r into those with m e g a c o l o n a n d those with
a n o r m a l sized colon. The latter g r o u p was further
divided into those with n o r m a l transit a n d those
with slow transit. T h e results were c o m p a r e d with
those r e c o r d e d f r o m 15 control subjects with norm a l bowel function. W i t h straining, anal pressure
fell in 12 o f 15 controls while in 3 it increased. In
30 o f 31 c o n s t i p a t e d patients, anal pressure rose
p a r a d o x i c a l l y with straining. E l e c t r o m y o g r a p h i c
recording in controls during straining d e m o n s t r a t ed decreased activity in 5, in 4 no change a n d in
5 an increase in activity. In 28 o f 31 c o n s t i p a t e d
patients E . M . G . activity increased with straining.
These results suggest t h a t external sphincter contraction during straining occurs in s o m e n o r m a l
subjects but m o r e frequently a m o n g patients with
c o n s t i p a t i o n o f different types.
Patients with chronic c o n s t i p a t i o n m a y be divided

into those with a n o r m a l sized c o l o n a n d those
with m e g a c o l o n , using c o n v e n t i o n a l b a r i u m e n e m a
studies [1]. T h o s e with a n o r m a l sized c o l o n m a y be
further divided b y m e a n s o f m e a s u r e m e n t o f intestinal transit rate into those with slow transit a n d
those w h o s e transit is within n o r m a l limits [2]. Previous studies h a v e suggested t h a t c o n s t i p a t e d patients in all these g r o u p s have difficulty in expelling
a rectal b a l l o o n [ 3 - 6 ] a n d t h a t this a b n o r m a l i t y
m a y be due to a failure o f relaxation o f the volunt a r y anal sphincters with defaecation.
In this study, the function o f the v o l u n t a r y ,

striated anal sphincters at rest, with v o l u n t a r y contraction a n d with d e f a e c a t i o n straining was tested
in a g r o u p o f severely c o n s t i p a t e d adults, all o f
w h o m could n o t expel a 50 ml w a t e r filled rectal
balloon. T h e results were c o m p a r e d with those obtained f r o m fifteen v o l u n t e e r subjects with n o r m a l
bowel function.
Methods
Patients
All patients studied had been referred with chronic constipation.
They underwent routine anorectal physiological tests and were
all found to be unable to expel a water filled rectal balloon.
Nineteen patients (mean age 37 years, range 14 64 years) had
a normal barium enema and all were female. Of these, 10 had
prolonged whole gut transit time and 9 had normal transit time.
Twelve patients (mean age 28 years, range 17-59 years) had
radiological evidence of megarectum [1]. Of these 9 were male
and 3 female.
Control subiects
Fifteen volunteer subjects were recruited from those attending
the colonoscopy clinic for the removal of colonic polyps or as
part of a polyp follow-up programme. They comprised 9 males
and 6 females with a mean age of 49 years (range 31-64 years).
All had a bowel frequency in the range of three motions per day
to three motions per week [7]. None of these patients reported
defaecation straining and all had a normal sized colon on barium enema. The control subjects selected were all able to expel a
water filled rectal balloon with effort.
Anal manornetry
Anal manometry was performed similarly in each group using a
micro-balloon technique [8] with the patient in the left lateral
position. Resting anal pressure was taken as the maximum pressure recorded in the anal canal, using a pull through technique.
Pressures measured during voluntary anal sphincter contraction
and voluntary defaecation straining were also taken from this
point. The recto-anal reflex was elicited in all subjects by infla-
208
275
tion of a balloon in the rectum and noting a fall in the resting

anal pressure [9].
250
225
Intra-rectal pressure
Intrarectal pressure was measured similarly in each group using
a microballoon placed in the rectal ampulla at a constant distance (8 cm) from the anal verge.
Electromyography
Anal
200
Manometry
crn/H20
175
~50
~25
100
75
Constipated patients had EMG activity recorded from the external sphincter, using an intramuscular concentric needle electrode [10]. Measurements were taken at rest and in response to
voluntary sphincter contraction and simulated defaecation
straining. Volunteer subjects were not submitted to needle EMG
testing but were examined with a surface bipolar plug electrode,
which was inserted to lie within the anal canal. Readings were
taken at rest, and during voluntary contraction and defaecation
straining. Integrated EMG activity recorded with the needle
electrode and the plug electrode could not be compared quantitatively but any increase or decrease above resting levels was
satisfactorily recorded using both techniques.
5O
25
I
Rest
Strain
Norrnals
Fig. 1. Anal pressure at rest and on defaecation straining in

control subjects and 17 constipated patients with a normal barium enema. Data not available in 2 of 19 patients
Table 1. Results in control subjects and patients with constipa-
tion with a normal barium enema and megarectum

Normals
15
Results
Anal manometry
M e a n resting a n a l p r e s s u r e in 15 v o l u n t e e r subjects
was 70 _+ 43 c m water. It rose o n v o l u n t a r y c o n t r a c t i o n in all subjects to a m e a n o f 1 7 0 + 7 2 c m water.
A n a l pressure fell d u r i n g d e f a e c a t i o n s t r a i n i n g in
12 o f 15 n o r m a l s ( m e a n 56 + 54 c m water) a n d rose
in 3 p a t i e n t s (Fig. 1) w h o also s h o w e d a n increase
in E M G activity o n straining.
I n the 19 p a t i e n t s with i d i o p a t h i c c o n s t i p a t i o n
a n d a n o r m a l b a r i u m e n e m a , m e a n resting a n a l
pressure w a s 73 _+ 27 c m water, a n d v o l u n t a r y c o n t r a c t i o n pressures 1 3 8 + 4 8 c m water. T h e pressure increased a b o v e resting levels d u r i n g d e f a e c a tion straining in 16 o f 17 p a t i e n t s tested ( m e a n
107_+ 28 c m water).
Twelve p a t i e n t s with i d i o p a t h i c m e g a r e c t u m
h a d a m e a n resting anal p r e s s u r e o f 65 _ 55 c m water, w h i c h rose to a m e a n o f 195_+82 c m w a t e r o n
v o l u n t a r y c o n t r a c t i o n . D e f a e c a t i o n straining p r o d u c e d a n increase in p r e s s u r e in all p a t i e n t s with
m e g a c o l o n to 150 + 87 c m water.
Intrareetal pressure
T h e m e a n i n t r a r e c t a l p r e s s u r e rose in all g r o u p s o n
straining (Table 1). It is interesting to n o t e t h a t the
a n a l p r e s s u r e in c o n s t i p a t e d p a t i e n t s d u r i n g straining was o f the s a m e o r d e r as the intrarectal pressure
achieved.
Rest
Strain
Constipated
Sex M : F
10:5
49
Mean age
126 _+45
Mean IRP
70 -+43
AP
R
SQ 170 _+72
ST 56 +54
2.8_+ 1.9"
EMG
R
SQ 10.7+_ 5.5
3.9-+ 3.1
ST
Constipated
Normal BE
19
Megarectum
12
0:19
9:3
37
28
100 _+44
181 +75
72 -+27
64 +44
138 -+47
195 _+82
107 -+28*
150 _+87*
5.4_+ 4.6"
8.3_+ 8.6 a
2 7 . 6 + _ 1 3 . 6 62.2_+62.0
1 6 . 5 _ + 1 0 . 0 42.8_+41.0
BE, Barium enema; R, rest; SQ, squeeze; ST, strain; IRP,

intrarectal pressure (cm/H20+SD); AP, anal pressure (cm/
H20 _+SD); EMG, integrated EMG (mV/s _+SD)
a It is not possible to compare the quantitative values between
normal and patient groups because a different electrode was
used (see text)
* Difference from normal p < 0.005 (unpaired t-test)
Electromyography
I n the c o n t r o l subjects the m e a n i n t e g r a t e d E M G
activity in the anal c a n a l at rest w a s 2.8 +_ 1.9 mV/s.
W i t h v o l u n t a r y c o n t r a c t i o n , activity increased in
all subjects to a m e a n i n t e g r a t e d value 1 0 . 7 +
5.5 m V / s . D u r i n g d e f a e c a t i o n straining (studied in
14 patients), a v a r i a b l e result w a s seen; 5 patients
s h o w e d decreased activity, 4 n o c h a n g e a n d 5 a
slight increase in activity.
I n 19 patients w i t h c h r o n i c c o n s t i p a t i o n a n d a
n o r m a l b a r i u m e n e m a , w h o were u n a b l e to expel a
rectal b a l l o o n , the m e a n resting i n t e g r a t e d E M G
activity was 5.4 + 5.6 m V / s . A c t i v i t y increased in all
p a t i e n t s o n v o l u n t a r y c o n t r a c t i o n to a m e a n inte-
209
grated activity o f 27.6-4-13.6 mV/s. M e a n activity
also increased during straining to 16.5 + 10.0 mV/s.
In 16 patients activity increased, in 2 it decreased
and in 1 no change was seen. In 12 patients with
idiopathic megarectum, m e a n resting activity was
8.3 + 6.0 mV/s rising to a m e a n o f 62.2 + 60 mV/s
with v o l u n t a r y contraction. Activity with defaecation straining rose in all o f these patients to a m e a n
o f 42.8 +41 mV/s.
Discussion
Different techniques were used for studying the
electrical activity o f the external sphincter muscles
in patients and control subjects for ethical reasons.
It can be argued that comparisons between the two
groups are invalid for this reason because the needle electrode is painful on insertion and the plug
electrode, used in the n o r m a l subjects, is painless
but could provide a stimulus to defaecation. H o w ever, no quantitative c o m p a r i s o n is m a d e between
the two types o f measurement. Further, the results
obtained c o r r e s p o n d closely with those o f anal
m a n o m e t r y p e r f o r m e d by an identical m e t h o d in
the control and patient groups.
In volunteer subjects, who were able to expel a
rectal balloon, a variable response in the electrical
activity o f the striated sphincters was seen with
defaecation straining. These findings s u p p o r t those
o f R u t t e r [11]. While 9 o f 15 control subjects (60%)
showed a decrease or no change in electromyographic activity, 5 o f 15 (33%) showed an increase
in activity in the v o l u n t a r y sphincter, despite being
able to expel a rectal ballon. These results suggest
that some people are able to expel rectal contents
t h r o u g h contracting sphincter muscles. This m a y
be the mechanism o f controlled passage o f flatus in
n o r m a l subjects and "social d e f a e c a t i o n " p r o p o s e d
by K e r r e m a n s [12].
N o n e o f the 31 constipated patients studied was
able to expel a rectal balloon and 28 had an increase in electrical activity in the v o l u n t a r y anal
sphincter during defaecation straining. It would
seem likely therefore that active c o n t r a c t i o n o f the
v o l u n t a r y sphincters plays a role in failure o f balloon expulsion in these patients.
Resting levels o f anal canal pressure were similar in controls and in b o t h patient groups. These
results are in agreement with the results o f Ihre [13]
and Lane [14]. With straining, levels o f anal pressure in the control g r o u p fell in all but 3 subjects.
In the 3 subjects with increased E M G activity, pressure in the anal canal decreased. This a p p a r e n t par a d o x m a y be explained by the fact that anal man o m e t r y records pressure p r o d u c e d by the concen-
tric activity o f b o t h the internal and external

sphincters. If the internal sphincter relaxes a fall in
pressure m a y be seen despite a weakly contracting
external sphincter.
In 30 o f 31 constipated patients unable to expel
a rectal balloon, anal pressure during straining rose
to levels that were higher than at rest. The pressure
during straining was also higher in constipated patients than controls (p < 0.005). The rise in pressure
is almost certainly due to the action o f the striated
muscle. This activity seems to occur b o t h in w o m e n
with a n o r m a l b a r i u m enema who show n o r m a l or
slow transit time and males and females with idiopathic megacolon. This study supports the n o t i o n
that a disorder o f sphincter function m a y be an
i m p o r t a n t factor in patients with constipation o f
different types.
References
1. Preston DM, Lennard-Jones JE, Thomas BM (1985) Towards a radiologic definition of idiopathic megacolon. Gastrointest Radiol 10:167-169
2. Hinton JM, Lennard-Jones JE, Young AC (1969) A new
method for studying gut transit time using radio opaque
markers. Gut 10:842-847
3. Barnes PRH, Lennard-Jones JE (1985) Balloon expulsion
from the rectum in constipation of different types. Gut
26:1049 1052
4. Preston DM, Lennard-Jones JE (1985) Anismus in chronic
constipation. Dig Dis Sci 30:413-418
5. Preston DM, Lennard-Jones JE, Thomas BM (1984) The
balloon proctogram. Br J Surg 71:29-32
6. Read NW, Timms JM, Barfield LJ, Donnelly TC, Bannister
JJ (1986) Impairment of defaecation in young women with
severe constipation. Gastroenterology 90:53-61
7. Wyman JB, Heaton KW, Manning AP, Wicks ACP (1978)
Variability of colonic function in healthy subjects. Gut
19:146-150
8. Hill JR, Kelly ML, Schlegel JF, Code CF (1960) Pressure
profile of the rectum and anus in healthy persons. Dis Colon
Rectum 3:203-209
9. Lawson J, Nixon HH (1967) Anal canal pressures in the
diagnosis of Hirschsprung's disease. J Paed Surg 2:544-552
10. Henry MM, Snooks SJ, Barnes PRH, Swash M (1985) Investigation of disorders of the anorectum and colon. Ann R
C Surg 67:355-360
11. Rutter KRP (1974) Electromyographic changes in certain
pelvic floor abnormalities. Proc R Soc Med 67:53-56
12. Kerremans R (1969) Morphological and physiological
aspects of anal continence and defaecation. Editions Arsica,
Brussels
13. Ihre T (1974) Studies on anal function in continent and
incontinent patients. Scand J Gastroenterol 9 [Suppl 25]
14. Lane RHS (1984) Internal sphincter dysfunction: a cause of
idiopathic megacolon. Dis Colon Rectum 27:577
Professor J. E. Lennard-Jones
St. Mark's Hospital
City Road
London ECIV 2PS
UK
Col6i c/al
Disease
Do patients with haemorrhoids have pelvic floor denervation?

C.E. Bruck, D.Z. Lubowski and D.W. King
Colorectal Clinic, St. George Hospital, Sydney, Australia
Abstract. Straining at stool is found in patients with

haemorrhoids, rectal prolapse and neurogenic
(idiopathic) faecal incontinence. In the latter two
conditions perineal descent and pudendal neuropathy occur. We have carried out anal manometry,
measurement of perineal descent, pudendal nerve
terminal motor latency (PNTML) and single fibre
E M G in the external anal sphincter in 16 patients
with haemorrhoids and 20 matched control subjects to determine whether patients with haemorrhoids have pudendal nerve damage. There was no
significant difference in resting or voluntary contraction pressures or in the incidence of slow waves
or ultra-slow waves between the patients with haemorrhoids and controls. There was a significant
difference between the groups in the position of the
perineum with respect to the ischial tuberosities
at rest (p<0.025) and on defaecation straining
(p<0.005). The mean P N T M L was higher in the
haemorrhoid group but this did not reach statistical significance (p = 0.07). The mean fibre density
was significantly higher in the haemorrhoid group
(p < 0.025). These findings show that patients with
haemorrhoids are more likely to have abnormal
perineal descent with pudendal neuropathy.
Abnormal descent of the pelvic floor on straining

was first described by Parks et al. [1], who suggested that rectal evacuation dysfunction could
lead to chronic straining at stool, abnormal perineal descent and, in some cases faecal incontinence. Straining at stool is frequently observed in
patients with haemorrhoids [2, 3], rectal prolapse
[4], the solitary rectal ulcer syndrome [5, 6] and
neurogenic (idiopathic) faecal incontinence [7-9].
The latter three conditions are associated with abnormal perineal descent and stretch-induced dam-
age to the pudendal nerves and pelvic innervation

of the external anal sphincter and pelvic floor musculature [4, 7-11].
The aim of this study was to determine whether
patients with haemorrhoids have pudendal nerve
damage and denervation of the external anal
sphincter muscle.
The study was carried out with approval from the St. George
Area Health Service Ethics Committee and with each patient's
informed consent.
Sixteen consecutive patients on the elective surgical waiting
list for haemorrhoidectomy were studied. There were 8 men and
8 women with a mean age of 55 years (range 22-71 years). A
careful history was obtained from each patient and details were
recorded on a standard proforma. Clinical features are shown in
Table 1. Surgery was indicated in 2 patients with moderate sized
first degree haemorrhoids because of continuing bleeding fol-
Table 1. Clinical features in 16 patients with haemorrhoids

No.
Bleeding
Prolapse
None
2nd degree
3rd degree
4th degree
Discomfort/pain
Pruritis
Chronic straining at stool
Continence
Normal
Minor leak
Major incontinence
Stress urinary incontinence
Mean duration of symptoms
16
2
3
10
1
12
5
11
11
5
0
1
6.7 yrs
(range 3 m - 2 0 yrs)
211
lowing sclerotherapy. Eleven of the 16 patients had intermittent
straining at stool. The mean length of history of straining was
11 years (range 4 30 years). Eight patients used laxatives regularly. The stool was hard or pellet-formed in 3 patients, loose in
one patient and the remaining 12 patients passed a formed stool
(aided by the use of laxatives in six). Five patients had minor
incontinence, consisting of a mucous discharge or intermittent
small smear.
Seven of the 8 women were multiparous and one was nulliparous. Four had undergone forceps delivery and one had a
failed trial of forceps followed by Caesarian section. Two patients had a prolonged second stage of labour (Table 2).
Twenty patients without anorectal disease were used as control subjects. They were age and sex matched, and the females
were matched as far as possible for parity and obstetric risk
factors (Table 2). There were 9 men and 11 women, mean age 52
years (range 27-76 years). Ten women had undergone vaginal
delivery and the remaining patient was delivered by elective
Caesarian section. The latter patient and one other were primiparous, and nine of the 10 women undergoing vaginal delivery
were multiparous; 5 of these had forceps-assisted delivery and 2
had a prolonged second stage of labour. None of the control
subjects had excessive straining at stool.
Anal manometry
Anorectal manometry was carried out using a closed water-filled
system with a micro-balloon 4 mm in diameter connected by a
non-distensible polyethylene tube to a pressure transducer and
recording apparatus (Devices MX-74). The lubricated probe
was passed into the rectum and withdrawn through the anal
canal and the maximal resting and voluntary contraction pressures were recorded. The presence of slow waves (15-40 per
minute) and ultra-slow waves (1 2.5 per minute) was noted.
Perineal descent
The position of the perineum was measured with respect to the
plane of the ischial tuberosities at rest and during a defaecation
straining effort using a perineometer [10, 12].
Table 2. Obstetric features in patients with haemorrhoids and

normal control subjects
No females
Vaginal delivery
Vaginal deliveries (median)
Forceps
Long 2nd stage (> 1 hr)
Large baby (> 9 lbs)
Patients
n =16
Controls
n = 20
8
6/8
2 (0-4)
4 + 1a
2
1
11
10/11
2 (1-6)
5
2
2
a One failed trial of forceps + Caesarian section
Table 3. Manometric and electrophysiological results in patients

with haemorrhoids and normal controls. Mean_+ SD
Patients
Controls
Resting pressure (cm H20 ) 68 + 19

63 _ 15
Voluntary contraction
(cmH20)
106_+92
87_+23
Perineal descent (cm)a
Rest
1.2_+1.0
1.7___0.5
Strain
-0.5-+_ 1.3 1.1 +__0.8
P N T M L (ms) b
2.0__+0.4 1.8+0.2
Fibre density
1.9-+0.6 1.5_+0.2
p
p
p
p
<
<
=
<
0.025
0.005
0.07
0.025
a Perineal position with respect to the plane of the ischial tuberosities

b PNTML, pudendal nerve terminal motor latency
Statistical analyses
Mean values were compared using the two-sample t-test. Individual values were considered to be abnormal if they exceeded
the mean normal value by more than 2 SD. Comparisons of the
frequency of observations were made using Fisher's exact probability test.
Pudendal nerve terminal motor latency ( P N T M L )

The P N T M L was measured as previously described [7, 10]. The
pudendal nerves were stimulated transrectally using a rubber
finger stall on which was mounted a stimulating and recording
electrode array. Square wave supra-maximal stimuli were delivered to the nerves at the ischial spines and the evoked compound
action potentials in the external anal sphincter muscle were
displayed on the oscilloscope screen and recorded on the paper
print-out (Neuromatic 2000, Dantec, Denmark).
Single-fibre electromyography (EMG)

The fibre density, a measure of re-innervation in denervated
striated muscle, was measured in the external anal sphincter
using a standard single-fibre needle electrode [8, 13]. The needle
was inserted into the external sphincter muscle on both sides,
making a total of 2 4 skin passes, and 20 consecutive reproducible action potentials were recorded.
Results (Table 3)
Perineal descent
There was a significant difference between the patient and control groups in the position of the perineum at rest (p<0.025). On straining the mean
position of the perineum in the patients and controls was 0.5+ 1.3 cm below the transischial line
and 1.1+-0.8cm above this line respectively
(p < 0.005). The perineal position on straining was
considered to be abnormal if it lay more than
0.5 cm below the level of the ischial tuberosities; 9
patients with haemorrhoids and one control subject
had abnormal perineal descent (p=0.001).
212
Discussion
3.0
2.5
0
0
Fibre
Density
2.0
ee
~o
1.5
00o
O0
000
O00
eae
Normsls
Hsemorrholds
p<0.025
Fig. 1. Fibre density in patients with haemorrhoids and normal

control subjects, e, Patients without abnormal perineal descent;
o, patients with abnormal perineal descent
Anorectal manometry
There was no significant difference in resting or

voluntary contraction pressures between the
groups. Slow waves were present in 9 patients and
11 controls (ns) and ultra-slow waves in 5 patients
and 4 controls (ns).
Pudendal nerve terminal motor latency
The mean P N T M L was higher in the patients but

this difference was not significant (p=0.07). The
P N T M L was raised ( > 2.2 ms) in 3 patients with
haemorrhoids and in a further two patients the
P N T M L was at the upper normal limit (2.2 ms).
Single-fibre E M G
The mean fibre density was significantly higher in

the patients than controls (p <0.025) (Table 3,
Fig. 1). The fibre density was raised (>1.9) in 8
patients and 2 control subjects (p =0.01).
Straining at stool results in abnormal pelvic floor

descent with stretching of the terminal portion of
the pudendal nerves, distal to the points at which
they are fixed near the ischial spines [14]. Chronic
straining at stool is a feature in patients with haemorrhoids [2, 3] and in this study eleven of the
sixteen patients reported straining. Nine patients
had abnormal perineal descent on straining and
there was a significant difference in the position of
the perineum on straining between the patient and
control groups.
Evidence that abnormal perineal descent is associated with denervation of the external anal
sphincter and puborectalis muscles was initially obtained from histometric studies in patients with
faecal incontinence [4]. Electrophysiological studies
subsequently confirmed these findings [7-11] and
the fibre density has been shown to be a sensitive
measure of pudendal neuropathy [13]. There was a
significant increase in fibre density in the patients
with haemorrhoids in this study.
Teramoto, Parks and Swash [15] observed muscle fibre hypertrophy in histometric studies of external anal sphincter muscle biopsies in patients
with haemorrhoids. Hypertrophy of external anal
sphincter muscle fibres is also found in patients
with neurogenic faecal incontinence [4]. However
other histological features seen in patients with
neurogenic faecal incontinence including fibre-type
grouping, atrophy and loss of muscle fibres, and
fibrosis were not observed in biopsies from patients
with haemorrhoids and the degree of muscle hypertrophy was less in the latter condition. Teramoto et
al. [15] concluded that the histological changes observed in patients with haemorrhoids were due to
work hypertrophy and not due to neuropathic
changes in the muscle. Using electrophysiological
techniques we have found evidence of pudendal
nerve damage in some patients with haemorrhoids
in this study. Indeed this would be expected since
nine of the sixteen patients had abnormal perineal
descent on straining which has previously been
shown to be associated with pudendal neuropathy
[7-11].
Threshold of anal mucosal electrosensitivity
has been used as a test of damage to the sensory
pathways of the pudendal nerves [16, 17] and a
raised threshold has been observed in patients with
neuropathic faecal incontinence [16, 17]. Bartolo et
al. [16] also observed a raised sensory threshold in
the upper anal canal in patients with haemorrhoids
and concluded that less sensitive mucosa may be
displaced downwards into the upper part of the
213
anal canal, in keeping with the theory of downward

displacement of anal submucosal cushions in this
condition. However it is possible that pudendal
neuropathy contributed to or even caused the rise
in sensory threshold in these patients.
Factors other than straining at stool may lead
to pudendal neuropathy. Vaginal delivery is an important cause of pelvic nerve damage and risk factors include forceps delivery, third degree perineal
tear and prolonged second stage of labour [18]. The
patient and control groups were therefore matched
for sex, parity and obstetric risk factors in this
study.
None of the five patients with incontinence had
true neurogenic incontinence. In each case the anal
pressures were within normal limits and there was
a minor leak related to the haemorrhoidal prolapse.
In contrast to previous studies on patients with
haemorrhoids [3, 19, 20] we did not find increased
resting anal pressures in our patients. Similarly the
incidence of ultra-slow waves was not higher than
in the control group. The latter finding is to be
expected since ultra-slow waves are observed more
frequently in subjects with high resting anal pressures [3, 19]. The absence of high resting pressures
in this study may reflect the nature of the cohort of
patients studied. Unlike other studies [19] all our
patients were awaiting haemorrhoidectomy. Eleven
of the sixteen patients (69%) had straining at stool
and nine patients (56%) had abnormal perineal
descent which may be a higher incidence than in
other studies [3, 19, 20] where the incidence was not
reported. Read et al. [20] showed that normal subjects and patients with the descending perineum
syndrome had lower resting anal pressures than
patients with haemorrhoids. We no longer regard
perineal descent as a syndrome [10], but rather as a
physical sign indicating weakness of the pelvic floor
musculature which is usually due to denervation.
Perineal descent and pelvic nerve damage may ultimately result in weakness of the internal [21] and
external anal sphincter muscles [8-11] and this may
have caused a fall in anal pressures to within the
normal range in the patients with haemorrhoids in
this study.
Faecal incontinence is a recognised complication of anal dilatation in the treatment of haemorrhoids [22, 23]. Incontinence is usually transient but
may be permanent and may be associated with internal or external anal sphincter damage [23]. Since
pelvic nerve damage with weakness of the anal
sphincter and pelvic floor musculature is an important cause of faecal incontinence, the results of this
study imply that anal dilatation may be contraindi-
cated in patients with haemorrhoids in whom there

is evidence of pudendal nerve damage.
Acknowledgements. We wish to thank Julie Hague and Kathy
Josey for their continued support, and Mr P. Gray, M.I.R.S.
Statistics and Information Co-ordinator, St. George Hospital
for carrying out the statistical analyses.
References
1. Parks AG, Porter NH, Hardcastle J (1966) The syndrome of
the descending perineum. Proc R Soc Med 59:477-482
2. Thomson JPS, Leicester RJ (1985) Haemorrhoids: pathophysiology and clinical features. In: Henry MM, Swash M
(eds) Coloproctology and the pelvic floor. Butterworths,
London, pp 195 209
3. Hancock BD (1977) Internal sphincter and the nature of
haemorrhoids. Gut 18:651 655
4. Parks AG, Swash M, Urich H (1977) Sphincter denervation
in anorectal incontinence and rectal prolapse. Gut
18:656-665
5. Rutter KR, Riddell RH (1975) The solitary ulcer syndrome
of the rectum. Clinics in Gastroenterol 4:505-530
6. Snooks SJ, Nicholls RJ, Henry MM, Swash M (1985) Electrophysiological and manometric assessment of the pelvic
floor in solitary rectal ulcer syndrome. Br J Surg
72:131-133
7. Kiff ES, Swash M (1984) Slowed conduction in the pudendal nerves in idiopathic (neurogenic) faecal incontinence. Br
J Surg 71:614-616
8. Neill ME, Parks AG, Swash M (1981) Physiological studies
of the anal sphincter musculature in faecal incontinence and
rectal prolapse. Br J Surg 68:531-536
9. Womack NR, Morrison JFB, Williams NS (1986) The role
of pelvic floor denervation in the aetiology of idiopathic
faecal incontinence. Br J Surg 73:404-407
10. Jones PN, Lubowski DZ, Swash M Henry MM (1987) Relation between perineal descent and pudendal nerve damage
in idiopathic faecal incontinence. Int J Colorect Dis
2:93-95
11. Bartolo DCC, Jarratt JA, Read MG, Donnelly TC, Read
NW (1983) The role of partial denervation of the puborectalis in idiopathic faecal incontinence. Br J Surg 70:664-667
12. Henry MM, Parks AG, Swash M (1982) The pelvic floor
musculature in the descending perineum syndrome. Br J
Surg 69:470-472
13. Neill ME, Swash M (1980) Increased motor unit fibre density in the external anal sphincter muscle in anorectal incontinence: a single fibre EMG study. J Neurol Neurosurg Psychiatry 43:343-347
14. Kiff ES, Barnes PRH, Swash M (1984) Evidence of pudendal neuropathy in patients with perineal descent and chronic
straining at stool. Gut 25:1279-1282
15. Teramoto T, Parks AG, Swash M (1981) Hypertrophy of
the external anal sphincter in haemorrhoids: a histometric
study. Gut 22:45-48
16. Roe AM, Bartolo DCC, Mortensen NJMcC (1986) New
method for assessment of anal sensation in various anorectal disorders. Br J Surg 73:310-312
17. Rogers J, Henry MM, Misiewicz JJ (1988) Combined sensory and motor deficit in primary neuropathic faecal incontinence. Gut 29:5-9
18. Snooks SJ, Swash M, Henry MM, Setchell MM (1986) Risk
factors in childbirth causing damage to the pelvic floor innervation. Int J Colorect Dis 1:20-24
214
19. Hancock BD, Smith K (1975) The internal anal sphincter
and Lord's procedure for haemorrhoids. Br J Surg
62: 833- 836
20. Read NW, Bartolo DCC, Read MG, Hall J, Haynes WG,
Johnson AG (1983) Differences in anorectal manometry
between patients with haemorrhoids and patients with
descending perineum syndrome: implications for management. Br J Surg 70:656-659
21. Lubowski RJ, Nicholls RJ, Burleigh DE, Swash M (1987)
Internal anal sphincter damage in neurogenic faecal incontinence. Dig Dis Sci 32:918
22. MacIntyre IMC, Balfour TW (1972) Results of the Lord
non-operative treatment for haemorrhoids. Lancet 1:1094
23. Snooks S, Henry MM, Swash M (1984) Faecal incontinence

after anal dilatation. Br J Surg 71:617-618

Dr. D. Z. Lubowski
St. George Hospital
Belgrave street
Kogarah
Syndey, NSW 2217
Australia
Col6reeial
Disease
Int J Colorect Dis (1988) 3:215 218
9 Springer-Vedag 1988
Relative risk of colorectal cancer after cholecystectomy

A multicentre case-control study
A. Mamianetti 1 R.O. Cinto 2, D. Altolaguirre 3, O.A. Bosicio 4 A. Heidenreich s and M. Salom6n 6
1 Department of Internal Medicine, Hospital Aeronfiutico Central, 2 Division of Statistics and Computer Sciences, National Institute
of Pharmacology and Bromatology, The Departments of Surgery at the following hospitals: 3Espafiol, 4Bonorino Udaondo,
5 Al6man and 6 Brit/mico, Buenos Aires, Argentina
Abstract. The relative risk of developing colorectal

cancer after cholecystectomy was assessed retrospectively in 493 patients with colorectal cancer
(239 women, 254 men). The results were compared
with a control group of patients matched for sex
and age. The overall relative risk was 0.7 (90%
confidence interval, 0.7-0.8). However, when the
data were analysed for site significant differences
were seen. In the caecum and ascending colon the
relative risk of developing colorectal cancer after
cholecystectomy was 2.8 (90% confidence interval,
1.0-9.4). In the rectum the relative risk was only
0.3 (90% confidence interval, 0.2-0.6) in both
sexes. The results suggest a relative increased risk of
developing right-sided colon cancer after cholecystectomy in women. However, they only partially
support the hypothesis that prior cholecystectomy
increases the relative risk of developing colorectal
cancer in view of the data relating to the the rectum.
There have been some clinical studies suggesting an association between large bowel cancer and
cholecystectomy. Capron et al. [10] compared the
frequency of prior cholecystectomy in 237 patients
operated on for colorectal cancer with 2,458 necropsy cases who were free of cancer. They found
that the frequency of prior cholecystectomy in
women with colorectal cancer was significantly
higher. Vernick et al. [11] subsequently indicated
that this association was between cholecystectomy
and right-sided colon cancer in both sexes.
In a previous retrospective study of 124 patients
with colorectal cancer and the matched controls we
found an increased relative risk of right-sided colon
cancer after cholescystectomy [12]. However, the
number of cases was small and in the present study
we set out to expand the series by incorporating the
participation of several hospitals in the city of Buenos Aires.

Bile acids and their metabolites are involved in the
aetiology of large bowel cancer [1]. Previous cholecystectomy promotes alterations of bile acid metabolism, leading particularly to an increased secondary bile acid concentration in bile and faeces
[2-4]. This could be due to an increase in enterohepatic recycling of bile acids thereby increasing
their bacterial enzymatic degradation. Secondary
bile acids may be cocarcinogenic and they have
been reported to promote colonic cancer in an experimental rat model [5, 6].
The effect of cholecystectomy on the development of carcinoma of the colon in mice was studied
by Werner et al. [7]. They induced tumours by subcutaneous injection of 1,2-dimethylhydrazin and
observed colonic carcinoma in 70% of the cholecystectomised animals, compared with 16% of controls. Others have obtained similar results [8, 9].
Basic details of patients with colorectal cancer including sex,

date of birth, date of cancer diagnosis, tumour site and date of
cholecystectomy if carried out were obtained from the case
records. All patients had had an histologically confirmed adenocarcinoma. They were grouped according to site of tumour as
follows: right-sided colon (caecum, ascending colon and proximal third of the transverse colon), left-sided colon (distal third
of the transverse colon and descending colon) and the sigmoid
colon and rectum. No identification of site could be made in
three cases. Using this division into three groups determined by
site it was possible to compare the present results with those
obtained in our previous study [12]. Subjects who had undergone cholecystectomy 6 months prior to diagnosis of colorectal
cancer were considered non-cholecystectomised.
Paired controls were identified from case records in the
same hospital as being cancer-free, and were matched for sex
and age (same or +_1 year). It was determined whether they had
been cholecystectomised or not.
The estimation of relative risk for colorectal cancer after
cholecystectomy was calculated according to the method described by Miettinen [13].
216
Results
ders this relative risk at t h a t site insignificant. A

low relative risk o f 0.4 in w o m e n a n d 0.3 in m e n
w a s u n e x p e c t e d l y o b s e r v e d in the r e c t u m . W h e n the
i d e n t i f i c a t i o n o f sex a n d site o f t u m o u r were n o t
stated the relative risk w a s 0.7 (90% c o n f i d e n c e
interval, 0 . 7 - 0 . 8 ) .
W h e n the d a t a were a n a l y s e d with p a t i e n t s
divided into the three g r o u p s a c c o r d i n g to site (Table 5) the h i g h e s t relative risk value was f o u n d in
the right c o l o n in w o m e n (2.2; 9 0 % c o n f i d e n c e interval, 0 . 9 - 5 . 8 ) .
T h e r e were 493 p a t i e n t s with c o l o r e c t a l c a n c e r

f r o m five h o s p i t a l s (Table 1) i n c l u d i n g 239 w o m e n
a n d 254 m e n . T h e m e a n age o f the w o m e n w a s
65.5 + 11.4 years a n d o f the m e n 6 2 . 4 _ 10.7 years.
O f the 493 patients, 47 ( 9 . 5 % ) h a d b e e n p r e v i o u s l y
c h o l e c y s t e c t o m i s e d . T h e s e i n c l u d e d 37 w o m e n a n d
10 m e n . O f the m a t c h e d c o n t r o l s , 66 ( 1 3 . 4 % ) h a d
b e e n c h o l e c y s t e c t o m i s e d i n c l u d i n g 46 w o m e n a n d
20 m e n . T h e incidence at different sites is s h o w n in
Tables 2 a n d 3. T h e c o l o r e c t a l c a n c e r relative risk
after c h o l e c y s t e c t o m y is s h o w n in Tables 4 a n d 5. It
was 2.8 ( 9 0 % c o n f i d e n c e interval, 1 . 0 - 9 . 4 ) in
w o m e n with p r o x i m a l c o l o n c a r c i n o m a . A l t h o u g h
a similar value o f 2 w a s f o u n d in the transverse
c o l o n , the wide c o n f i d e n c e interval o f 0 . 2 - 5 7 . 9 ren-
Discussion
Table 1. Number ofcentres and number of cancer-control pairs
Centres
Hospital
Hospital
Hospital
Hospital
Hospital
Number of
cancer-control
pairs
Aeronfiutico
Alemfin
Britfinico
Espafiol
Udaondo
Total
124
139
44
96
90
493
T h e d i s t r i b u t i o n o f t u m o u r s w i t h i n the large b o w e l
(Table 3) w a s similar to t h a t r e p o r t e d b y E v a n s
et al. [14] in a n e p i d e m i o l o g i c s t u d y p e r f o r m e d in
the U n i t e d States o f A m e r i c a .
We h a d p r e v i o u s l y r e p o r t e d a relative risk o f
c h o l e c y s t e c t o m y in c o l o r e c t a l c a n c e r p a t i e n t s o f 7
in b o t h sexes f o r the right-sided colon. W i t h larger
n u m b e r s in the p r e s e n t study, this has fallen to 2.2
f o r w o m e n a n d to 1 f o r m e n in the right colon.
T h e r e a p p e a r s to be a difference b e t w e e n the sexes
s h o w n p a r t i c u l a r l y in Table 4 in w h i c h for p a t i e n t s
w i t h t u m o u r s in the c a e c u m a n d a s c e n d i n g c o l o n ,
relative risks o f 2.8 a n d 0.5 f o r females a n d males,
respectively, were f o u n d . This is similar to the risk
o f 2.1 o b t a i n e d b y L i n o s et al. [15] in w o m e n with
right-sided c o l o n cancer, in a f o l l o w - u p s t u d y o f
Table 2. Incidence of prior cholecystectomy in cancer-control pairs
Site of cancer
No. of patients
Age: mean (years)
range (years)
Incidence of cholecystectomy
Cancer
Age"
Right-sided
Left-sided
Sigmoid colon
and rectum
Total
n = 100
= 68.3
R = 42- 93
n = 42
=62.5
R=41-79
n =351
~ = 62.8
R=16 94
n = 493
=63.9
R = 16-94
Controls
No. of
patients
Time b
Age
X = 15.5
R = 2-40
= 62.6
R=39-83
~ =5
R=5-5
=66.5
R = 54-72
2 = 15.7
R=l-41
=66.0
R=51-81
~ =15.2
R = 1-41
= 65.2
R=39 83
n = 19
~ = 76.4
R = 56-93
" Age when cancer was diagnosed

b Interval between cholecystectomy and cancer diagnosis
c Interval between cholecystectomy and the moment when cancer were diagnosed in the pair
=18.7
R=2-34
n=49
n = 47
~ =71.1
R = 37-93
=7.8
R=l-17
n=5
n=26
~ = 66.9
R=37-84
Time c
n=12
n= 2
~ =76
R=74-78
No. of
patients
=12.4
R = 1-29
n=66
=11.9
R = 1-34
217
Table 3. Incidence of prior cholecystectomy in colorectal cancer
patients and control subjects
Site of Tumour
Number
Caecum
Ascending colon
Transverse colon
Descending colon
Sigmoid colon
Rectum
42
38
40
22
128
223
Total
493
Percent
8.5
7.7
8.1
4.4
26.0
45.2
Incidence of
cholecystectomy
Cancer
Control
9
6
5
1
15
11
7
2
4
4
19
30
47
66
Table 4. Relative risk with 90 per cent confidence interval by sex

and tumour site
Site of cancer
Women
Men
Women
and men
Caecum
2.0
0.6-7.2
0
0-3.5
1.3
0.5 3.9
Caecum and ascending

colon a
2.8
1.0-9.4
0.5
0.0-6.3
2.0
0.8 5.4
Transverse colon
1.0
0.2 5.5
2.0
0.2 57.9
1.3
0.3-4.9
Descending colon
0.3
0.0 3.0
0
0 19
0.3
0.0-1.9
Sigmoid colon
0.7
0.3-1.7
0.8
0.2-3.0
0.8
0.4-1.5
Rectum
0.4
0.1 0.8
0.3
0.1-0.9
0.3
0.2-0.6
No site difference
0.8
0.6 1.2
0.5
0.2-1.0
0.7
0.7-0.8
a Miettinen's index estimate was calculated for caecum and

ascending colon together. Ascending colon index could not be
calculated separately since its denominator was zero
Table 5. Relative risk and 90% confidehce interval by sex and
tumour site
Kuller in a retrospective study [16]. An increased

relative risk for right-sided colon cancer was reported by Turunen and Kivilaakso [17]. Narisawa
et al. [18] found a positive association between
right-sided colon cancer and previous cholecystectomy. Others [10, 19, 20] have also indicated
that previous cholecystectomy increases the relative
risk of right-sided colon cancer in women only.
However, these findings have not been confirmed
in other studies [21-25] in which prior cholecystectomy was not associated with an increased
risk of developing right-sided colon cancer.
The unexpected finding of a relative risk significantly lower than one in rectal cancer for both men
and women was also observed by Adami et al. [23]
but in women only.
Secondary bile acids have been reported to increase following cholecystectomy [2-4], and it has
been postulated that this increases the risk of colonic cancer. In a study of 18 patients with gallstones and a normal functioning gallbladder secondary bile acids did not change after cholecystectomy [26]. This suggested that secondary bile
acids were associated with gallstones and the risk
factor for colorectal cancer could thus be gallstones
rather than cholecystectomy. An association between colorectal cancer and gallstones was reported by Lowenfels [27] but this was not found by
Linos et al. [28].
If prior cholecystectomy increases the relative
risk of developing right-sided colon cancer, it might
be expected to be higher in women than in men.
Perhaps, as suggested in animal studies [29], sex
steroid hormones may be involved in colonic cancer.
The results obtained in this study suggest an
increase of the relative risk of developing rightsided colon cancer in women and a decreasing risk
of developing cancer in the rectum in both sexes.
However, they only partly support the hypothesis
that prior cholecystectomy increases the relative
risk of colorectal cancer and prospective clinical
studies should be carried out.
Site of cancer
Women
Men
Women
and men
Right-sided colon
2.2
0.9-5.8
1.0
0.2-5.5
1.8
0.8-3.9
Acknowledgements. The authors wish to thank Pedro Streeton,
Left-sided colon
0.5
0.1-2.7
0
0-19
0.4
0.1-1.9
M.D. and Mrs. Sheilah Steeton for technical assistance and Mr.
Mario Bergamalli for his financial aid.
Sigmoid colon and rectum
0.5
0.3-0.9
0.4
0.2-1.0
0.5
0.4-0.8
1,681 cholecystectomised subjects over a period of

about 14 years. In our study the relative risk of
right-sided colon cancer in both sexes was 1.8, similar to the value of 1.86 reported by Vernick and
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1. Lacassagne A, Buu-Hoi NP, Zajdela F (1961) Carcinogenic
activity of apocholic acid. Nature 190:1007-1008
2. Almond HR, Vlahcevic SR, Bell CC Jr, Gregory DH, Swell
L (1973) Bile acid pool kinetics and biliary lipid composition
before and after cholecystectomy. N Engl J Med
289:1213-1216
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3. Malagelada JR, Liang VW, Summerskill WHJ, Gamble WS
(1973) Bile acid secretion and biliary bile acid composition
altered by cholecystectomy. Am J Dig Dis 18:455-459
4. Pomare EW, Heaton KW (1973) The effect of cholecystectomy on bile salt metabolism. Gut 14:753-762
5. Narisawa T, Magadia NE, Weisburger JH, Wynder EL
(1974) Promoting effect of bill acids on colon carcinogenesis
after intrarectal instilation of N-methyl-N'-nitro-Nnitrosoguanidine in rats. J Natl Cancer Inst 53:1093-1097
6. Reddy BS, Watanabe K, Weisburger JH, Wynder EL (1977)
Promoting effect of bile acids in colon carcinogenesis in
germ-free and conventional F344 rats. Cancer Res
37:3238-3242
7. Werner B, deHeer K, Mitschke M (1977) Cholecystectomy
and carcinoma of the colon. Z Krebsforsch 88:223-230
8. Schattenkerk ME, Li AKC, Jeppsson BW, Eggink WF,
Jamieson CG, Ross JS, Malt RA (1980) Cholecystectomy
has no influence on frequency of chemically induced colonic
cancer in mice. Br J Cancer 42:791-793
9. Narisawa T, Sano M, Sato M, Takahashi T, Tanida N,
Shimoyama T (1985) The correlation between cholecystectomy and fecal bile acis and large-bowel cancer induced with 1,2-Dimethylhydrazine in mice. Dis Colon Rectum 28:27-30
10. Capron JP, Delamarre J, Canarelli JP, Brousse N, Dupas JL
(1978) La cholecystectomie favorise-t-elle l'apparition du
cancer rectocolique? Gastroenterol Clin Biol 2:383-389
11. Vernick LJ, Kuller LH, Lohsoonthorn P, Rycheck RR,
Redmond CK (1980) Relationship between cholecystectomy and ascending colon cancer. Cancer 45:392-395
12. Mamianetti A, Cinto RO, Lafont D (1983) Colecistectomia
y adenocarcinoma colorectal. Acta Gastroent Lat Am
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(1978) Management and survival of carcinoma of the colon.
Ann Surg 108:716-720
15. Linos DA, Beard CM, O'Fallon WM, Dockerty MB, Beart
RW, Kurland LT (1981) Cholecystectomy and carcinoma of
the colon. Lancet 2:379-381
16. Vernick LJ, Kuller LH (1981) Cholecystectomy and rightsided colon cancer: an epidemiological study. Lancet
2:381-383
17. Turunen M J, Kivilaakso EO (1981) Increased risk of colorectal cancer after cholecystectomy. Ann Surg 194:639- 641
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19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
cancer in low-risk Japanese population. Dis Colon Rectum

26:512-515
Alley PG, Lee SP (1983) The increased risk of proximal
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Moorehead R J, Kernohan RM, Patterson CC, McKelvey
STD, Parks TG (1986) Does cholecystectomy predispose to
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Weiss NS, Daling JR, Chow WH (1982) Cholecystectomy
and the incidence of cancer of the large bowel. Cancer
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Abrams JS, Anton JR, Dreyfuss DC (1983) The absence of
a relationship between cholecystectomy and the subsequent
occurrence of cancer of the proximal colon. Dis Colon Rectum 26:141-143
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U-B (1983) Colorectal cancer after cholecystectomy: absence of risk increase within 11 -14 years. Gastroenterology
85:859-865
Blanco D, Ross RK, Paganini-Hill A, Henderson BE (1984)
Cholecystectomy and colonic cancer. Dis Colon Rectum
27:290-292
Eriksson SG, Lindstr6m CG (1984) Lack of relationship
between cholecystectomy and colorectal cancer. Scand J
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Linden W van der, Katzenstein B, Nakayama F (1983) The
possible carcinogenic effect of cholecystectomy. Cancer
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Monk MA, Sternby NH (1982) Cholelithiasis, cholecystectomy and cancer: a case-control study in Sweden.
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Linos DA, O~
WM, Thistle JL, Kurland LT (1982)
Cholelithiasis and carcinoma of the colon. Cancer
50:1015-1019
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project summary of the 1979 workshop: approaches to prevention and treatment of large bowel cancer. Cancer
45:1264-1271

Dr. A. Mamianetti
Hospital Aeronautico Central
Ventura de la Vega 3697
(1437) Buenos Aires
Republica Argentina
Col6reclal
Disease
Effect of ketanserin, a selective antiserotoninergic drug,

on human anal canal pressure*
M. Neri**, L. Marzio, C. De Angelis, O. Pieramico, A. Mezzetti and F. Cuceurullo
Institute of Medical Physiopathology, University of Chieti, Chieti, Italy
Abstract. T h e effect o f K e t a n s e r i n , a n e w a n t i s e r o t o n i n e r g i c d r u g , o n h u m a n a n a l p r e s s u r e in v i v o
was investigated. Anal pressure was recorded
c o n t i n u o u s l y in 14 n o r m a l s u b j e c t s b y a l o w compliance water perfused probe with two recordi n g p o i n t s a t t h e s p h i n c t e r level. A f t e r a 3 0 - m i n
b a s a l t r a c i n g K e t a n s e r i n (10 m g I V as b o l u s ) o r
p l a c e b o w a s a d m i n i s t e r e d in a d o u b l e b l i n d
m a n n e r , a n d t h e r e c o r d i n g c o n t i n u e d f o r 1 h. T h e
r e s u l t s s h o w t h a t K e t a n s e r i n i n d u c e d a 3 0 % fall in
a n a l p r e s s u r e s o o n a f t e r its a d m i n i s t r a t i o n w h i c h
was statistically significant when compared with
t h e p l a c e b o ( p < 0 . 0 1 ) . T h i s effect l a s t e d u p t o
40 m i n o f r e c o r d i n g a n d w a s f o l l o w e d b y a r e t u r n
t o c o n t r o l v a l u e s w i t h i n 1 h.
Of various pharmacological influences that may

a f f e c t i n t e r n a l a n a l s p h i n c t e r t o n e , it h a s b e e n
s h o w n t h a t 5 - h y d r o x y t r y p t a m i n e ( 5 - H T ) in l o w
c o n c e n t r a t i o n is c a p a b l e o f i n d u c i n g c o n t r a c t i o n in
m u s c l e s t r i p s o f h u m a n i n t e r n a l a n a l s p h i n c t e r [1].
K e t a n s e r i n ( J a n s s e n , B e l g i u m ) , a d r u g w i t h selective a n t i s e r o t o n i n e r g i c a c t i o n , h a s r e c e n t l y b e e n
d e v e l o p e d a n d h a s b e e n u s e d in t h e t r e a t m e n t o f
hypertension and bronchospasm.
In the present investigation we have studied the
effect o f K e t a n s e r i n o n a n a l c a n a l t o n e t o see
whether this may be modified by an antiseroton i n e r g i c d r u g in v i v o .
* Part of this work has been presented to the Xth International
Symposium on Gastrointestinal Motility, Rochester, MN,
USA, 1985
** Present address: Gastroenterology Unit, Mayo Clinic, Rochester, MN 55905, USA
Materials and Methods

Fourteen normal subjects (10 male, 4 female, mean age 35 10,
ranging from 16 to 56 years) have been studied. All subjects gave
their informed consent to the study, and manometry was performed after excluding disease of the anal canal by sigmoidoscopy.
Anal manometry was performed using a low compliance
water perfused catheter with distal side openings, connected to
a pressure transducer. The probe comprised three catheters (ID
0.9 mm, OD 1 mm) inserted into a rigid cannula (OD 4 mm).
Two side openings were located 5 cm from the tip, oriented
radially and perfused continuously at the rate of 0.5 cc/min with
distilled water from a pressurized infusion bottle. Intraluminal
pressures were measured by pressure transducers (Statham,
Puerto Rico, P230 b), inserted into each infusion line and connected to an eight channel polygraph recorder (Beckman R612).
The third catheter terminated in a small latex balloon (4 x 4 cm),
located at the tip of the probe.
The assembly was advanced through the anal canal until
rectal pressure was recorded. It was then gradually withdrawn at
approximately 1 mm/s and the maximum pressure during this
rapid pull through (RPT) was recorded. The rectoanal inhibitory reflex was checked by computing the decrease from maximal
pressure that was obtained by the inflation of the balloon at
10 ml increments of air up to 200 ml, with distension maintained
for 30 s.
The decrease, calculated at each balloon inflation, proved
to be within the normal range as previously published [2]. After
identifying the rectoanal inhibitory reflex, a 30-rain basal control period of anal canal pressure was then obtained by reinserting the probe into the rectum and slowly withdrawing it until a
plateau pressure had been reached. The probe was then taped to
the buttocks and recording was continued during saline intravenous infusion. After the 30-min control period, Ketanserin
10 mg IV as bolus (seven subjects), or placebo in a form identical
to the drug (seven subjects), was given randomly in a double
blind fashion and recording was continued for I h. In three more
cases a rapid pull through pressure recording was obtained
30 min after the administration of the drug, and both the maximum decrease of pressure was observed and the rectoanal inhibitory reflex was studied.
The highest value recorded at each minute was calculated,
and for each 10-min period a mean value was computed. Student's t-test for paired data was used to compare the three
220
100-
Placebo
1
--
80
.... I _ _ L - i
-I-
--
tl
....... I__I
60-
,_ 40Q.
20 9
- o-1'o
la
2'0
Minufes
Fig. 1. Line graphs of the effect of the administration of Ketanserin, 10 mg IV, or placebo (arrows) on h u m a n internal anal
sphincter (IAS) pressure; sphincter tone decreases soon after the
drug injection and gradually returns to basal within one hour.
Asterisks indicate statistical significance vs placebo (p < 0.001)
10-min periods preceding the drug infusion with each 10-min

period afterwards. Values are expressed as mean the standard
deviation,
Results
During the 30-min basal tracing obtained in the

14 subjects mean anal canal resting pressure was
63.2_+6.2mm Hg (Fig. 1). Following infusion of
Ketanserin anal canal basal pressure fell to
32 + 9 mm Hg within 5 _+2 min. This decrease continued within each four 10-min period after the
administration of the drug with the greatest fall
occurring at the end of the second period. Injection
of the placebo did not modify the baseline recording (Fig. 1).
In the three subjects in whom a second rapid
pull through was done at 30 min after Ketanserin,
the decrease of anal canal pressure was significant
(basal RPT 86.7 _+29.8 mm Hg, 30 min RPT
58.8_+37.1 m m Hg; t=5.006, p<0.003). The rectoanal inhibitory reflex in the same subjects showed
a 30% reduction in the pressure decrease following
rectal distension and this paralleled the fall in the
baseline anal canal pressure recording following
Ketanserin. At the end of the four 10-min periods
following Ketanserin, a gradual increase of anal
canal resting tone occurred with a return to basal
pre-Ketanserin values within I h.
Discussion
The study has shown that the administration of

Ketanserin, a specific serotonin antagonist, induces
a 30% fall in basal anal tone with a peak fall at
around 30 min and a return to baseline within I h.

It is known that the internal anal sphincter
spontaneously maintains a high resting tone in vitro [3, 4] and in vivo [5, 6]. While in vitro tone seems
to be myogenic since it is not affected by tetrodotoxin [7], in vivo tone may be modulated by a variety of neural or pharmacological influences [8].
It has been proposed that 5-HT may regulate
gastrointestinal motility since it is found in enteric
neurons, is released after stimulation and mimics
the action of enteric nerves [9]. Contraction of the
anal sphincter following compression of the bladder has been observed in the cat and is abolished by
dihydroergotamine [8], a serotoninergic antagonist,
and 5-HT has been shown to contract human internal anal sphincter muscle strips in vitro by a direct
action on the smooth muscle cell [7]. There are
however no data on the possible role of 5-HT in
regulating human anal pressure in vivo.
Ketanserin is a well known antiserotoninergic
drug acting mainly on the 5 - H T 2 type receptors
which have been shown to be present along the
gastrointestinal tract [10, 11]. It is thought that
serotoninergic neurons function as excitatory interneurons in the gut [12], and induce a transmitter
release [8]. The inhibition of anal canal tone by
Ketanserin in the present study suggests a role for
the serotoninergic system in maintaining the
sphincter tone at rest in humans.
Pharmacological evidence suggests that anal
canal resting tone is partly due to tonic sympathetic
discharge [13]. Infusion of metoxamine, an alphaagonist, in normal subjects increased anal canal
tone while the administration of phentolamine, an
alpha-blocker, markedly inhibited it. Since a partial alpha-antagonist action has been recently described for Ketanserin [14], it could be speculated
that the fall in anal canal tone after Ketanserin
observed in this study is due, at least in part, to the
inhibition of an excitatory sympathetic tone. However, the effects of Ketanserin on blood vessel
smooth muscle in humans were present also in the
absence of evident alpha adrenergic blockade [15]
and studies in animals have shown that the tonic
alpha-adrenergic activity is not responsible for the
resting tone of the internal anal sphincter [16].
Since we did not measure the effect of Ketanserin on external anal sphincter function, it is possible
that the reduction in resting anal pressure was due
to an action on this muscle. However, it is known
that the selective paralysis of the external anal
sphincter by pudendal block or muscle relaxant
produces only a slight diminution of anal pressure
[4, 17]. It is also reported that the internal anal
sphincter contributes 75% to 85% of the resting
221
pressure in the anal canal [4, 18] and that internal

sphincterectomy markedly reduces anal pressure [3,
19]. Furthermore, there is no reported evidence that
this antiserotoninergic drug affects striated muscle.
Thus a direct effect on the external sphincter would
seem unlikely.
In conclusion this work suggests that the serotoninergic system may play a role in maintaining
internal anal sphincter tone. In addition the data
suggest a role for Ketanserin in the treatment of
disease associated with increased anal canal pressure such as idiopathic constipation resulting from
outlet obstruction [20], anal fissure [21, 22], symptomatic haemorrhoids [23, 24] and chronic anal
pain.
References
1. Burleigh ED, D'Mello A (1983) Neural and pharmacological factors affecting motility in the internal anal
sphincter. Gastroenterology 84:409-417
2. Marzio L, Lanfranchi GA, Bazzocchi G, Cuccurullo F
(1985) Anorectal motility and rectal sensitivity in chronic
idiopathic constipation: effect of high fiber diet. J Clin Gastroenterol 7:391-399
3. Bennett RC, Duthie HL (1964) The functional importance
of the internal anal sphincter. Br J Surg 51:355-357
4. Frenckner B, Euler C von (1975) Influence of pudendal
block on the function of the anal sphincters. Gut
16:482 489
5. Ustach TJ, Tobon F, Hambrecht T, Bass DD, Schuster MM
(1970) Electrophysiological aspects of human sphincter
functions. J Clin Inv 49:41 48
6. Wankling WJ, Brown BH, Collins CD, Duthie HL (1968)
Basal electrical activity in the anal canal in man. Gut
9:457-460
7. Burleigh DE, D'Mello A, Parks AG (1979) Responses of
isolated human internal anal sphincter to drugs and electrical field stimulation. Gastroenterology 77:484-490
8. Christensen J (1981) Motility of the colon. In: Johnson LR
(ed) Physiology of the gastrointestinal tract. Raven Press,
New York, pp 445 471
9. Gershon MD (1982) Serotoninergic neurotransmission in
the gut. In: Polak JM, Bloom SR, Wright NA, Butler AG
(eds) Structure of the gut. Page Bros, Norwich, pp 205-219
10. Gohtert M, Schlicker E (1987) Classification of serotonin
receptors. J Cardiovasc Pharmacol 10 [Suppl 3]:$3-$7
11. Davidson HI, Pilot MA, Thompson HI-I (1986) 5hydroxytryptamine stimulates canine gastrointestinal motility via a 5-HT receptor mechanism. In: Abstract and Programme of the 3rd European Symposium on Gastrointestinal Motility, Bruges, p 75
12. Wood JD (1981) Physiology of the enteric nervous system.
In: Johnson LR (ed) Physiology of the gastrointestinal tract.
Raven Press, New York, pp 1-37
13. Gutierrez JA, Shah AN (1975) Autonomic control of the
internal anal sphincter in man. In: Vantrappen G (ed) Vth
International Symposium on Gastrointestinal Motility. Typoff Press, Belgium, pp 363-373
14. Robertson JIS, Stott DJ, Ball SG (1987) Antihypertensive
mode of action of Ketanserin. J Cardiovasc Pharmacol 10
[Suppl 3]:$45-$47
15. Brouwer RML, Wenting GJ, Man in't Veld AJ, Schalekamp
MADH (1987) Role of alpha-adrenergic blockage in the
cardiovascular action of Ketanserin: studies of patients with
essential hypertension, autonomic insufficiency, and Raynaud's phenomenon. J. Cardiovasc Pharmacol 10
[Suppl 3]:$26-$31
16. Culver J, Rattan S (1986) Genesis of anal canal pressures in
the opossum. Am J Physiol 251:G765-G771
17. Frenckner B, Ihre T (1976) Influence of autonomic nerves
on the internal anal sphincter in man. Gut 17:306-312
18. Schweiger M (1979) Method for determining individual
contributions of voluntary and involuntary anal sphincters
to resting tone. Dis Colon Rectum 22:415-416
19. Duthie HL, Watts JM (1965) Contribution of the external
anal sphincter to the pressure zone in the anal canal. Gut
6:64-68
20. Martelli H, Devroede G, Arhan P, Duguay C (1978) Mechanisms of idiopathic constipation: outlet obstruction. Gastroenterology 75:623-631
21. Hancock BD (1977) The internal anal sphincter and anal
fissures. Br J Surg 64:92-95
22. Gibbons CP, Read NW (1986) Anal hypertension in fissures: cause or effect? Br J Surg 73:443-445
23. Deutsch AA, Moshkowitz M, Nudelman I, Dinari G, Reiss
R (1987) Anal pressure measurements in the study of hemorrhoid etiology and their relation to treatment. Dis Colon Rectum 30:855-857
24. Hiltunen K, Matikainen M (1985) Anal manometric findings in symptomatic hemorrhoids. Dis Colon Rectum
28:807-809
Dr. M. Neri
Istituto di Fisiopatologia Medica
Ospedale SS. Annunziata
1-66100 Chieti
Italy
Col6i ee/al
Disease
Ulcerative colitis in a developing country of Africa:

the Baragwanath experience of the first 46 patients
I. Segal
Gastroenterology Unit, Baragwanath Hospital and the University of the Witwatersrand, Johannesburg, South Africa
Abstract. Ulcerative colitis is reported to be rare in

black populations o f sub-Saharan Africa. This series o f the first 46 patients treated at B a r a g w a n a t h
Hospital, Soweto, indicates that most patients
(72%) presented with severe s y m p t o m s and extensive colonic involvement. There is a p a r a d o x o f
severe extensive disease yet relative lack o f complications requiring surgery. This is p r o b a b l y due to
the modification o f the natural history o f the disease t h r o u g h medical treatment, particularly corticosteroid therapy. T h e r e is a long delay between
onset o f s y m p t o m s and diagnosis (3 years). Ulcerative colitis affects mainly women. The m e a n age o f
presentation is 36 years. Patients are urbanised and
m o s t belong to the u p p e r educational group while
a significant p r o p o r t i o n are in the higher occupational categories. Follow-up is p o o r with only one
third o f patients regularly attending the outpatients d e p a r t m e n t once the disease is controlled.
Ulcerative colitis is u n c o m m o n in sub-Saharan Africa. Only 18 cases were reported prior to 1975
[1-6]. In developing countries the a p p a r e n t rarity
o f the disease could be attributed to: (1) lack o f
medical personnel and special diagnostic facilities,
(2) difficulty in m o n i t o r i n g continuity in the care o f
the individual patients, (3) the sketchy nature o f
medical records, and (4) the relative c o m m o n n e s s
o f other causes o f b l o o d y diarrhoea.
In Soweto, some o f these difficulties were overcome in 1975 with the establishment o f a gastroenterology unit with specialised diagnostic facilities
at B a r a g w a n a t h Hospital. This hospital with 2740
beds, is the largest in Africa. The total n u m b e r o f
patients treated by the gastroenterology unit in
1987 was 4523.
Background
The black p o p u l a t i o n o f Soweto is a p p r o x i m a t e l y
2 million and comprises members o f all tribal
groups in South Africa. It is a complex polyglot
p o p u l a t i o n and includes those u r b a n b o r n and bred
and immigrants who have been there f r o m 2 0 - 5 0
years and short term migrants. It is mainly lower
working class but includes emerging highly urbanised, better trained, u p p e r - w o r k i n g and middle
classes [7].
This p a p e r describes the first 46 patients with
ulcerative colitis diagnosed by the gastroenterology
unit.

All patients diagnosed since 1975 have been included in this
study. The diagnosis of ulcerative colitis was made on the basis
of the following: 1. Amoebiasis, shigellosis, tuberculosis, bilharziasis, Yersinia enterocolitica, U venereum and Crohn's disease
were considered in the differential diagnosis and excluded by
laboratory investigations for these diseases.
2. Despite negative tests for amoebiasis (serology, microscopy of stools and histology of rectal biopsy specimens) all patients received a trial of metronidazole therapy.
3. Clinical, radiologic, sigmoidoscopic and histologic evidence was consistent with the diagnosis of ulcerative colitis.
All patients had barium enemas and 34 had colonoscopies
in order to determine the extent of the disease.
The grading of severity of colitis was based on the classification of Truelove and Witts [8, 9]. Thus severe disease was
present if more than 6 diarrhoeal stools were passed per day,
constitutional signs were present, the haemoglobin value was
less than 10 g/dl and the ESR was above 30 mm/h. Mild disease
was characterised by less than 4 stools per day, no constitutional
signs, anaemia or a raised ESR. Moderately severe disease occurs between these 2 grades.
Proctitis was defined as inflammation up to 15 cm from
the anal margin, rectosigmoiditis as inflammation up to the
sigmoid/descending colon junction, and extensive colitis as involvement of the rest of the colon but not necessarily the whole
223
colon. The term total colitis refers specifically to involvement of
the whole colon, including the ascending colon.
Results
The 46 patients had the following characteristics:
Clinical features
Sex and age. There were 34 women and 12 men
( F : M =2.8: 1). The mean age at presentation was
35.6 years (range 8 - 6 2 years). Most patients were
in the 20-39 year old age group. The age distribution at presentation is shown in Table I.
Symptoms at presentation. All patients presented
with bloody diarrhoea. In addition, 32 patients
(70%) had weight loss. Two patients presented with
pyoderma gangrenosum. Most patients were very
ill on admission to hospital. The clinical types classified according to severity indicated that 5 patients
(11%) had mild disease, 10 (22%) moderately severe disease and 31 (67%) severe disease. No patients presented with toxic megacolon or perforation. There were no deaths during hospital treatment.
Clinical course. 40 patients (87%) on follow-up had
a relapsing-remitting type of clinical course. 30 patients (65%) experienced mild recurrent attacks,
whereas 10 (22%) had severe recurrent attacks.
Two patients had continuous disease. The clinical
course in 4 patients was unknown as they did not
return for follow-up after discharge from hospital.
Delay between onset of symptoms and diagnosis. The
median delay between onset of disease and diagnosis was 3 years (range 1 month to 21 years).
Table 1. Age distribution of patients presenting for the first time

with ulcerative colitis
Age (years)
No. of patients
< 10
11-19
20-29
30 39
40-49
50-59
6O +
1
2
15
13
10
3
2
2
4
33
28
22
7
4
Table 2. Haemoglobin values at presentation
Normal (above 14 G%)

Values between 1 0 . 5 - 1 4 G %
Values between 8-10.5 G %
Values below 8 G %
Unknown
No. of patients
6
6
13
18
3
13
13
28
39
7
Thus 67% presented with severe iron deficiency

anaemia (haemoglobin values below 10.5 g/dl).
Complications. Sclerosing cholangitis occurred in 4

patients and pyoderma gangrenosum in 3 patients.
The diagnosis of sclerosing cholangitis was based
on clinical and biochemical evidence of jaundice,
pruritis, cholestasis and a raised alkaline phosphatase. ERCPs showed the typical features of irregularity and beading of the intrahepatic and extrahepatic biliary tree. Liver biopsies were consistent
with the diagnosis of sclerosing cholangitis. There
were 2 deaths. One patient died after developing an
ileo-femoral thrombosis and in one patient the
cause of death was unknown.
Social factors
Distribution of disease at presentation. Fifteen

(33%) presented with total colitis; 18 (39%) with
extensive colitis, 10 (22%) with rectosigmoiditis
and 1 with proctitis. In 2, the distribution was not
known. Thus the majority of patients (72%) presented with severe disease.
Haemoglobin values at presentation (Table 2). Six
patients had normal haemoglobin values. The
remainder (except for 3 in whom the haemoglobin
values are not known) presented with iron deficiency anaemia. 18 (39%) had values below 8 g/dl; 13
(28 %) had values between 8-10.5 g/dl and 6 (13 %)
had haemoglobin values between 10.5-14g/dl.
Habitat. Forty-three patients (93%) were urban

born, and 3 (7%) were born in a rural area.
Education (Table 3). 31 (67%) went to high school,
and 11 (24%) had only primary school education;
1 had no education. The educational status of 3
(7%) was unknown. The patients were better educated than the average Sowetan black of whom
18% had no schooling, 55% had primary school
education and 27% high school education [10].
Occupations (Table 4) [11]. Nine patients (23%)
were in professional or management occupations
224
Table 3. Educational status of ulcerative colitis patients compared with Sowetans
Education
Ulcerative colitis
patients (%)
Sowetans
(%)
High school
Primary school
No schooling
Unknown
67
24
2
7
27
55
18
Table 4. Occupational status of ulcerative colitis patients compared to economically active Sowetans (11)
Occupation
Professional and
managerial
Skilled
Semi-skilled
Unskilled
Administrative and
clerical
Other
Unknown
Ulcerative colitis
patients (%)
Sowetans
(%)
22.5
17.5
17.5
32.5
6
6.5
28.7
34.6
5
5
6.3
18.2
6 scholars in ulcerative colitis group not included
compared with 6% of Sowetans. Seven patients

(17.5%) were skilled workers compared with 6.5%
of Sowetans. Thus, although the series of ulcerative
colitis patients is small, a significantly greater number were in higher occupational categories than the
general Sowetan population. Six patients who were
scholars were excluded from the analysis.
Discussion
Ulcerative colitis and Crohn's disease are the most

common chronic intestinal bowel diseases in western populations [12]. In contrast to western populations ulcerative colitis is supposedly rare in black
populations of sub-Saharan Africa. Recent reports
however have shown that it has emerged as a definite disease entity in the urban South African black
[13, 14].
In the context of Africa, where infections are
probably the commonest cause of bloody diarrhoea, a query may arise as to the certainty of the
diagnosis. In this series, ulcerative colitis was a diagnosis of exclusion and was only accepted after
other diseases, mentioned in the Methods section,
were excluded. In addition, the natural history was
consistent with ulcerative colitis and patients responded to specific treatment for ulcerative colitis.
The above study indicates that the disease is

more common in women. The mean age of onset is
36 years. Patients are urbanised and in the main
belong to the upper educational strata of a population in a developing country. A significant proportion are in the higher occupational categories compared with the general population of Soweto. It
must be noted however that most patients are
semiskilled or unskilled workers.
The urban bias may be due to the fact that the
hospital serves a predominately urban community.
It is possible that the disease occurs in rural areas
but is either not diagnosed or reported.
The diagnosis of ulcerative colitis was made at
a very late stage - approximately 3 years after the
onset of symptoms. Severe iron deficiency anaemia
was common (67%). Chronic bloody diarrhoea
was the presenting complaint in all the patients,
and was accompanied by weight loss in most. The
vast majority of patients (89%) presented with
moderately severe or severe disease. In addition
72% had either total colitis or extensive colitis. Yet
the short term prognosis was excellent. No patient
developed toxic megacolon or perforation and no
patient died during hospital admission. Also, in
most patients (65%) the clinical course was characterised by being the mild relapsing-remitting type.
A possible explanation for the paradox of severe
disease and a mild clinical course is that treatment
has modified the natural history of the disease and
altered the morbidity and mortality of ulcerative
colitis. Evidence indicates that the cumulative mortality in ulcerative colitis has been reduced by almost 50% since the advent of steroid therapy in the
1950s. It is in the acute attack of moderate disease
in which steroids have unquestionably increased
the chance of temporary remission or improvement
[15].
The bias towards a severe presentation probably indicates that patients with mild disease do not
come to hospital. Thus, the incidence of the disease
in the black community may be greater than is
suggested by this series. It is noteworthy that
Wright from Cape Town [9] reported that 75% of
coloured patients with ulcerative colitis also presented with moderate/severe disease.
Sclerosing cholangitis was the commonest
extra-intestinal complication (4 patients) followed
by severe pyoderma gangrenosum (3). There were
2 deaths in the series and 3 patients had proctocolectomies.
Follow-up of the patients has presented difficulties. Most do not return to the out-patients department once the disease is controlled, except for acute
attacks. In fact, only 34% of the patients still attend
225
r e g u l a r l y for f o l l o w - u p . I n view o f the p o s s i b l e h i g h
risk o f c o l o r e c t a l c a n c e r i n this g r o u p it m a y b e
a d v i s a b l e to offer p a t i e n t s w i t h e x t e n s i v e disease
e a r l y surgery, p a r t i c u l a r l y since s p h i n c t e r s a v i n g
o p e r a t i o n s are n o w feasible.
Acknowledgement. The author wishes to acknowledge the support of the Chairman's Fund, Anglo-American and De Beers
Education Trust, for this study.
References
1. Billinghirst JR, Welchman JM (1966) Idiopathic ulcerative
colitis in the African: a report of 4 cases. Br Med J
1:211-213
2. Pillay VKG (1964) Ulcerative colitis in the African. Br Med
J 2:689
3. Sealay BJ, Gelfand M (1968) Ulcerative colitis in an African. Cen Aft J Med 14:173-175
4. Sobel JD, Schamroth L (1970) Ulcerative colitis in the
South African Bantu. GUT 11:760-763
5. Spencer SS, Nhonoli AM (1972) Ulcerative colitis in East
Africans. East Aft Med J 49:163-169
6. Awori NW, Rees PH, Roy AD (1972) Causes of chronic
diarrhoea in Kenya and their relationship to ulcerative colitis. East Afr Med J 49:604 613
7. Segal I, Dubb AA, Ou Tim L, Solomon A, Sottomayor MC,
Zwane EM (1978) Duodenal ulcer and working class mobility in an African population in South Africa. Br Med J
1: 469-472
8. Truelove SC, Witts LJ (1955) Cortisone in ulcerative colitis.

Br Med J: 1041-1048
9. Wright JP (1986) The epidemiology of inflammatory bowel
disease in Cape Town, 1980 1984. S Afr Med J 70:10-15
10. Bureau of Market Research (1982) Income and expenditure
patterns of urban black multiple households in Johannesburg, 1980. Research Report No. 94.7. University of South
Africa, Pretoria
11. Bureau of Market Research (1976) Income and expenditure
patterns of urban black households in Johannesburg. Research Report No 50.3. University of South Africa, Pretoria
12. Gilat T, Grossman A, Bujanover Y, Rozen P (1982) Epidemiology of inflammatory bowel disease. State of the art
and aetiologic inferences. In: Rachmilewitz D (ed) Inflammatory bowel disease. Martinus Nijhoff, The Hague,
pp 143-151
13. Segal I (1982) Inflammatory bowel disease in black populations of sub-Saharan Africa. Trop Gastro 3:15-22
14. Segal I (1984) Intestinal tuberculosis, Crohn's disease and
ulcerative colitis in an urban black population. S Afr Med
J 65:37-44
15. Cello JP (1983) Ulcerative colitis. In: Sleisenger MH, Fordtran JS (eds) Gastrointestinal disease. WB Saunders, Philadelphia, pp 1122-1168
Professor I. Segal
Gastroenterology Unit
Baragwanath Hospital
PO Bertsham 2013
Johannesburg
South Africa
Col6i'eeial
Disease
Review
Pouchitis
G. N. J. Tytgat and S. J. H. van Deventer
Department of Gastroenterology, Academic Medical Center, Amsterdam, The Netherlands
The continent ileoanal anastomosis with construction of a reservoir or pouch, has proven to be a
useful alternative for proctocolectomy and ileostomy [1, 2]. Immediate postoperative complications
consist of pelvic infection and obstruction which
have been reported to occur in 10% of operated
patients [3]. The mortality of the procedure is very
low [4] and long term functional results are generally gratifying, as spontaneous evacuation as well as
continence can be achieved in the majority of patients with a J-shaped reservoir [5, 6]. Recent modifications in the surgical technique, including the
introduction of four-loop (W) pouches have further
improved the quality of life after restorative proctocolectomy [7-9]. Restorative proctocolectomy
has therefore become an attractive alternative to
conventional ileostomy or colectomy followed by
ileorectal anastomosis in patients with adenomatous polyposis or severe ulcerative colitis.
However, as experience with the continent
ileoanal anastomosis has grown, it has become evident that inflammation of the mucosa of the ileal
reservoir known as 'pouchitis' might become a
major long term complication [10, 11]. Pouchitis
has been reported to occur in 7 - 4 2 % of patients at
risk [3, 4]. During a follow-up ranging from 6 to 62
months after proctocolectomy of a large series of
patients, pouchitis, based upon endoscopic and histological criteria, developed in 11% [12]. The symptomatology of pouchitis is characterized by frequent painful stooling, bloody diarrhoea, urgency
of defaecation, and sometimes fever. Patients typically complain of malaise, and in some cases symptoms can be observed which are reminiscent of the
systemic complications of inflammatory bowel disease. For instance, we recently observed three cases
with refractory arthritis, and reappearance of pyoderma gangrenosum lesions in one patient.
A definitive diagnosis is usually made endoscopically. The spectrum of endoscopic findings

comprises local erythema, scattered punctiform
haemorrhages, and focal superficial ulceration, but
in severe cases ulcers may become deep (Fig. 1).
These abnormalities may be limited to the pouch,
or spread over a certain distance in the prepouch
ileum. In some patients aphthous lesions may
mimic Crohn's disease, and an original diagnosis of
ulcerative colitis may be thought to have been erroneous. However, there is no doubt that Crohnlike lesions can develop in ileoanal reservoirs of
patients operated for genuine ulcerative colitis.
Histologically, some degree of chronic inflammation and villous atrophy occur in a high percentage of patients, usually without concurrent macroscopic changes of the ileal reservoir [12, 13]; pouch
ileum shows a tendency for colonic-type metaplasia. Occasionally, fibromuscular obliteration of the
lamina propria, and crypt basal hyperplasia may
mimic the histological findings of the solitary ulcer
syndrome. These chronic inflammatory changes
are observed in pouches from patients with ulcerative colitis, as well as those with adenomatous
polyposis, and do not correlate with the clinical
result [14]. When pouchitis is diagnosed endoscopically, histological evidence of acute inflammation is
invariably present, i.e. neutrophil infiltration, crypt
abscesses and ulceration. These findings are very
similar to the features seen in active ulcerative colitis, and indeed ileal-anal pouchitis is far more
common in patients operated for ulcerative colitis
than after colectomy for adenomatous polyposis [6,
13]. Likewise with the Kock continent ileostomy,
pouchitis has been reported to occur exclusively
after colectomy for ulcerative colitis [15].
Little is yet known about the pathogenesis of
pouchitis. Anaerobic overgrowth, due to faecal
227
Fig. 1. a Ileoanal pouch lined with normal looking small bowel mucosa, with Kerckring folds, b Mild pouchitis characterized by focal
erythema and friability, c Severe pouchitis, characterized by confluent erythema and widespread ulceration
stasis, has been suggested as a possible pathogenic

factor [16]. One study showed an inverse correlation between the presence of volatile fatty acids
derived from anaerobic bacteria and the degree of
villous atrophy in the pouch ileum [17]. It was suggested that these volatile acids might suppress the
growth of bacteria that produce toxic metabolites.
Quantitative cultures of the faecal content of ileoanal pouches did not reveal a higher number of
anaerobes in patients with pouchitis, compared
with controls without histological evidence of acute
inflammation [14]. Of course, these findings do not
rule out qualitative changes in the bacterial flora in
patients with pouchitis. Interestingly, backwash
ileitis diagnosed prior to colectomy, does not seem
to be a risk factor for later development of pouchitis [18]. The recent finding that in some patients
pouch mucin histochemically resembles colon mucin (as opposed to small bowel mucin) [13] might
prove to be pivotal, because it is well known that
colon mucin from patients with ulcerative colitis
differs from normal subjects [19]. Perhaps this abnormal mucin is more permeable for toxins present
in the bowel lumen, resulting in inflammation. A
candidate toxin, present in large quantities in the
gut is endotoxin [20], which is a potent inducer of
a host of inflammatory mediators including interleukin 1, tumour necrosis factor, and platelet activating factor [21, 22]. The observation that oral
administration of kaopectate, an endotoxin-binding substance, can reverse pouchitis lends support
to this hypothesis [16, 23]. Alternatively, the dedifferentiated pouch mucosa might become vulnerable to various immunological mechanisms, as was
the original colonic mucosa. Whatever hypothesis

might prove to be correct, investigations on pouchitis may unravel pathogenic mechanisms that
also are of importance in ulcerative colitis.
Little is known about the efficacy of medical
treatment of pouchitis. Although some investigators reported metronadizole to be effective [4], at
present no controlled trials have been performed to
support this impression. Furthermore, as discussed
above, the rational basis for this treatment is now
uncertain. Inflamed pouches that evacuate incompletely should be drained. We have occasionally
treated patients with severe pouchitis with corticosteroids and 5-amino salicylic acid with success,
but experience with this type of therapy is limited.
The ultimate outcome of pouchitis is unknown.
It is uncertain how many patients operated for ulcerative colitis will eventually develop pouchitis, or
whether the disease will permanently subside in
those affected. At present, the necessity to remove
the pouch, with conversion to a conventional ileostomy, the ultimate failure, is extremely uncommon.
Nevertheless, studies on the pathogenesis of pouchitis are much needed. For comparison of histological findings, a scoring system for acute and
chronic changes has been proven to be useful [4].
However, basic knowledge of the pathogenesis of
inflammation of the pouch mucosa is almost completely lacking. We therefore suggest that future
study should include investigation of recently identified mediators that have been shown to play an
important role in the induction of inflammation in
the bowel mucosa. For instance, platelet-activating
factor (PAF) has been shown to mediate endo-
228
toxin-induced damage to the intestinal mucosa [22],

but the role of PAF as a local mediator of intestinal
inflammation has yet not been investigated.
13.
14.
References
1. Parks AG, Nicholls RJ, Belliveau P (1980) Proctocolectomy
with ileal reservoir and anal anastomosis. Br J Surg
67:533-538
2. Utsunomiya J, Iwama T, Imaho M, Matsuo S, Sawai S,
Yaegashi K, Hirayama R (1980) Total colectomy, mucosal
proctectomy and ileoanal anastomosis. Dis Colon Rectum
23:459-466
3. Dozois RR (1985) Ileal 'J' pouch-anal anastomosis. Br J
Surg 72 [Suppl]: 80-82
4. Dozois RR, Goldberg SM, Rothenberger DA, Utsunomiya
J, Nicholls RJ, Cohen Z, Hulten LAG, Moskowitz RL
(1986) Symposium: Restorative proctocolectomy with ileal
reservoir. Int J Colorect Dis 1:2-19
5. Taylor BM, Cranley B, Kelly KA, Phillips SF, Beart RW,
Dozois RR (1983) A clinico-physiological comparison of
ileal pouch-anal and straight ileoanal anastomosis. Ann
Surg 198:462-468
6. Nicholls RJ, Moskowitz RL, Shepherd NA (1985) Restorative proctocolectomy with ileal reservoir. Br J Surg
72 [Suppl]: 76-79
7. Nicholls RJ, Pezim ME (1985) Restorative proctolectomy
ileal reservoir for ulcerative colitis and familial adenomatous polyposis: a comparison of three reservoir designs. Br
J Surg 72:470 474
8. Nicholls RJ, Lubowski DZ (1987) Restorative proctocolectomy: the four loop (W) reservoir. Br J Surg 74:564-566
9. Harms BA, Hamilton JW, Yamamoto DT, Starling JR
(1987) Quadruple-loop (W) ileal pouch reconstruction after
proctocolectomy: analysis and functional results. Surgery
102:561-567
10. Nicholls RJ, Belliveau P, Neill M, Wilks M, Tabaqchali S
(1981) Restorative proctocolectomy with ileal reservoir: a
pathophysiological assessment. Gut 22:462-468
11. Mortensen N (1988) Progress with the pouch-restorative
proctocolectomy for ulcerative colitis. Gut 29:561-565
12. Moskowitz RL, Shepherd NA, Nicholls RJ (1986) An
assessment of inflammationin the reservoir after restorative
15.
16.
17.
18.
19.
20.
21.
22.
23.
proctocolectomy with ileoanal ileal reservoir. Int J Colorect

Dis 1:167 174
Shepherd NA, Jass JR, Duval I, Moskowitz RL, Nicholls
RJ, Morson BC (1987) Restoratove proctocolectomy with
ileal reservoir: pathological and histochemical study of
mucosal biopsy specimens. J Clin Pathol 40:601-607
O'Connell PR, Rankin DR, Weiland LH, Kelly KA (1986)
Enteric bacteriology, absorption, morphology and emptying after ileal pouch-anal anastomosis. Br J Surg 73:909
-914
Hulten L, Svaninger G (1984) Facts about the Kock continent ileostomy. Dis Colon Rect 27:553-557
Fonkalsrud EW (1984) Endorectal ileoanal anastomosis
with isoperistaltic ileal reservoir after colectomy and
mucosal proctectomy. Ann Surg 199:151-157
Nasmyth DG, Godwin PGR, Dixon MF, Williams NS,
Johnston D (1985) The relationship between mucosal structure and intestinal flora in ileal reservoirs. Br J Surg 72:129
Gustavsson S, Weiland L, Kelly KA (1987) Relationship of
backwash ileitis to ileal pouchitis after ileal pouch-anal
anastomosis. Dis Colon Rect 30:25-28
Podolsky DK, Isselbacher KJ (1983) Composition of human colonic mucin. J Clin Invest 72:142-153
Van Deventer SJH, ten Cate JW, Tytgat GNJ (1988) Intestinal endotoxemia. Clinical significance. Gastroenterology
94:825 831
Cybulsky MI, Chan MKW, Movat HZ (1988) Biology of
disease. Acute inflammation and microthrombosis induced
by endotoxin, interleukin-1, and tumor necrosis factor and
their implication in Gram-negative infection. Lab Invest
58:365-378
Wallace JL, Steel G, Whittle BJR (1987) Evidence for
platelet-activating factor as a mediator of endotoxininduced gastrointestinal damage in the rat. Gastroenterology 93:765-773
Ditter B, Urbaschek R, Urbaschek B (1983) Ability of various absorbents to bind endotoxins in vitro and to prevent
endotoxemia in mice. Gastroenterology 84:1547-1552
Professor G. N. J. Tytgat
Department of Gastroenterology
Academic Medical Center
Meibergdreef 9
NL-1105 AZ Amsterdam
The Netherlands
Jo.m.,o+
Coi6i'eetal
Disease
Int J Colorect Dis (1988) 3 : 2 2 9 - 2 3 1
Current practice
The lost polyp: a guide to retrieval during colonoscopy
J.D. Waye, B.S. Lewis, M.A. Atchison and M. Talbott
Abstract. Polyps resected during colonoscopy
should be recovered and sent for pathologic examination. Unfortunately retrieval is incomplete ranging from 85-100% in reported series. There are
several specific techniques aimed to increase the
retrieval rate which in our experience amounted to
94.5% of a series of 182 polypectomies in 100 consecutive patients. All lost polyps were small and
were thought to have been aspirated through the
suction channel of the endoscope. In our study
10% of the initially "lost" polyps were within the
instrument prior to cleaning. Various forms of
polyp retrieval are reviewed with special attention
to locating the aspirated polyp.
The authors' experience
Many resected polyps never find their way into the

pathology laboratory for a histologic diagnosis.
There are many reasons for not retrieving colonoscopically resected polyps. They include small
lesions aspirated through the suction apparatus
into a large "catch-bottle", those that fragment
upon being suctioned through the collection
tubing, and polyps lost within the colon either in a
pool of fluid or hidden in some crevice.
There are various techniques available for the
location and retrieval of colon polyps after resection. Special attention is required to recover polyps
small enough to be aspirated through the biopsysuction channel. Meticulous application of recovery methods is necessary to locate polyps which
lodge in the colonoscope and might be lost during
post-polypectomy instrument cleaning.
From February to May 1987 data were collected on 100 consecutive patients having colonoscopic examinations in whom 182 polyps were
removed, 36 by the hot biopsy and 146 by the cautery snare technique. Of these, 172 (94.5%) polyps
were retrieved. Of the 146 polyps resected by snare,
104 were aspirated through the biopsy port of the
instrument, 13 polyps were removed still attached
to the snare and 27 were removed by suction to the
colonoscope tip while removing the instrument.
Twenty-eight polyps were not found initially after
being aspirated through the biopsy port. A meticulous search located 18 of these. Eleven were found
on aspirating water through the instrument after
the endoscopic examination. Three were found in
the black rubber protective cap over the biopsy
port which can be inspected directly on removing
the black rubber protective "splash-guard" and
looking at its under surface. Three polyps were
found after removal of the suction button by passing a brush through the biopsy channel of the instrument and pushing the polyps out of the tip. One
was found by directing the brush into the umbilical
of the instrument. Thus, of the 94.5% of polyps
recovered by various techniques, 10% were found
only after a meticulous search of the instrument
following colonoscopy.
Methods of retrieval
Retrieval rates of colonoscopically resected polyps

by experienced endoscopists are reported to be
85-100%. Spencer reported a retrieval rate of
83.5% in a series of 158 polypectomies [1]. In a
larger series, Wolff and Shinya recovered 93.2%
(574/616) [2] and Kitano retrieved 94.3% of polyps
(483/512) [3]. Webb reported the highest retrieval
rate, 97.9%, in 1000 polypectomies [4]. Kitano
noted that the retrieval rate fell as the number of
polyps resected during the colonoscopy increased
and as the size of the polyps decreased [3]. All the
230
lost polyps in our series were small and thought to
have been aspirated through the suction apparatus.
Early techniques such as using enemas of one to
two litres administered through the colonoscope
and collecting the specimen in a bedpan [5] have
been abandoned in favour of the techniques described above.
The hot biopsy technique permits polyp resection and certain retrieval in one manoeuvre. Once
a polyp has been grasped and fulgurated with the
hot biopsy forceps, the forceps can be withdrawn
and the specimen successfully retrieved from its
jaws. The tissue within the biopsy forceps is preserved for subsequent histopathologic examination
with only 1 in 500 specimens artifactually distorted
by the electrical current [6]. Unfortunately, polyps
larger than 0.8 mm in diameter cannot be removed
by this technique.
Polyps removed by snare polypectomy must
first be located after excision to be retrieved. Frequently they fall by gravity outside the field of vision after division of the pedicle and are difficult to
find. Under this circumstance the endoscopist may
not be sure whether the endoscope should be advanced or withdrawn to locate the polyp. There is
however a simple technique that will invariably
help to locate the polyp by flushing 15 to 30 cc. of
water via a syringe into the biopsy port while
watching the flow of water [7]. If a steady stream of
water is seen, this indicates that the tip of the instrument is facing in a dependent position, with the
water flowing away from the instrument. The colonoscope must then be advanced along the direction of flow of water to find the polyp. If, on the
other hand, the water injection causes a blurred
appearance across the lens, then the instrument tip
must be facing upward, and the endoscope must be
withdrawn. In either event, the endoscopist must
aspirate the first pool of water encountered subsequently to find the resected specimen. If a considerable amount of fluid is present in the colon, this
task may be somewhat difficult and the operator
may not be sure that a small polyp has not already
passed through the suction port.
A polyp larger than 8 mm in diameter can be
retrieved by a variety of techniques. The most reliable method is to regrasp it with a snare and withdraw the endoscope with the tip of the snare holding the polyp approximately 3 to 5 cm from the
viewing port enabling visualization of the distal
colon during extubation [5, 7]. The polyp is pulled
close to the instrument tip as the colonoscope is
withdrawn through the anus to prevent its dislodgement at this point of retrieval. Aspiration of a
large polyp to the instrument tip is another highly
successful form of retrieval [8-10]. With the polyp

so held to the colonoscope tip, vision is obscured
and thus, after removing the endoscope, it is necessary to reinsert the instrument to the level of the
polypectomy to check removal. If two polyps are to
be withdrawn, they can both be captured within a
single wire snare application. Snug closure of the
snare on the first polyp will enable it to remain
impacted while the snare is reopened to lasso the
second polyp. Closure of the snare loop may then
enable both to be retrieved. If more than two
polyps are to be retrieved the "long-nose polyp
retriever" (Microvasive Incorporated) may be useful. This non-electric device resembles a regular
snare loop with a long narrow proboscis at its tip.
Once a polyp is encircled, closure of the snare handle places the retrieved polyp at the end of the
proboscis. It will stay in that position when the
snare handle is again opened so that the widest part
of the loop can be placed over a second polyp which
will also slide down the proboscis as closure is effected. In this manner, three or four polyps may be
successfully recovered. The three-pronged retriever
is a difficult instrument to use and frequently tears
the polyps. The wire Dormia basket is not suitable
for retrieval of polyps.
Polyps less than 8 mm in diameter may be amenable to suction through the biopsy port (2- 8 ram)
of a standard colonoscope. The suction distorts the
tissue such that a round 8 mm polyp will appear to
be narrower and more elongated that it was in-situ.
When aspirating a polyp with this technique, it is
important to place the suction port of the instrument (located in the 5 o'clock position on Olympus
endoscopes) immediately over the polyp. Larger
polyps of the villous adenoma type may be more
compressible than the compact tubular adenoma,
and comparatively larger pieces may be retrieved
by suction aspiration.
Recovery of small polyps aspirated within a
standard suction receptable varying from 250 to
2500 ml may be an onerous task. Approximately 10
years ago we began to collect small specimens in a
standard mucus-trap designed for bronchoscopic
aspiration placed on the suction port of the instrument. Water suction directed the specimen into a
trap of only 50 ml volume. It was thus considerably
easier to find small polyps by straining the liquid
from this smaller trap instead of searching through
a much larger container.
More recently we have developed a new disposable polyp-retrieval trap specifically designed for
collection of colonoscopically resected small
polyps. This trap (EndoDynamic, Inc., Westbury,
NY) has four separate collection areas with a grid
231
under surface of the cap the lost polyp may be seen

resting on the rubber surface, or the polyp may
sometimes be seen within the metal portion of the
port previously covered by the cap. The third step
entails passing a cleaning brush retrograde through
the instrument from the biopsy port. The tip of the
instrument should be held over a specimen pot
since the polyp may be ejected from the channel by
the brush. Once the brush tip has emerged from the
instrument, the bristles should be inspected to ensure that the polyp has not been trapped there. If
the instrument has the capability, a brush should
be passed through the suction channel and out
through the umbilical where the suction tubing attaches. The final and last step for the search for the
lost small polyp is another aspiration of a large
volume of water once the instrument has been
reassembled.
References
Fig. 1. The new disposable multiple polyp retrieval trap (EndoDynamic Inc., Westbury, NY)
in each compartment (Fig. 1). Specimens from various sites may be captured separately within each of
the four small cups, by rotating a different collection area under the stream of aspirated fluid. The
grid permits total tissue retrieval of one or several
specimens without the need to strain any of the
aspirated colonic fluid which flows through the
grid into the main collection container. Even small
fragments of polyps of 1 - 2 mm will be collected by
this method.
When aspirated small specimens are not found
within the recovery trap or suction container, the
polyp is likely to be found in one of five different
places. The search should follow a set pattern and
should begin with flushing water through the endoscope with the suction trap attached. The force of
water may bring the polyp through the channel and
into the trap. The second manoeuvre is to remove
the rubber cap covering the biopsy port. On the
1. Spencer R J, Coates HL, Anderson MJ (1974) Colonoscopic

polypectomies. Mayo Clinic Proc 49:40-43
2. Wolff WI, Shinya H (1974) Modern endoscopy of the alimentary tract. Curr Probl Surg 11:1-62
3. Kitano H, Nogaki M (1983) Colonoscopic polypectomy
with special reference to management of multiple polyps.
Gastroenterol Endosc 25:883-889
4. Webb WA, McDaniel L, Jones L (1985) Experience with
1000 colonoscopic polypectomies. Ann Surg 201:626-632
5. Shinya H (1982) Colonoscopy: diagnosis and treatment of
colonic diseases. Igaku-Shoin, New York, pp 191-194
6. Williams CB (1973) Diathermy-biopsy, a technique for
the endoscopic management of small polyps. Endosc
5:215-218
7. Waye JD, Geenen J, Fleischer D, Venu R (1987) Techniques
in therapeutic endoscopy. Saunders, Philadelphia,
pp7.15 7.16
8. Overholt BF (1975) Colonoscopy: a review. Gastroenterol
68:1308-1320
9. Maas LC, Gelzayd EA, Doyle PJ (1984) Polyp retrieval
impossible without colonoscope tip (letter). Gastrointest
Endosc 30:378
10. Ricca JJ, Ahmed MM (1977) Retrieval of polyps severed at
colonoscopy (letter). Gastrointest Endosc 24:44
J. D. Waye, M. D.
650 Park Avenue
New York, NY 10021
USA
Coloi'eclal
Disease
Correspondence
Rectal sensation, the rectoanal reflex, and faecal incontinence
Dear Sir,
There is some confusion in the literature and in the

minds of physiologists regarding the normal cause
of internal sphincter relaxation, and the nature
and significance of the rectoanal inhibitory reflex.
Hancke and Schurholz [1] investigated rectal sensation and the inhibitory reflex in controls and patients with faecal incontinence. They noted that the
volume of water in an intrarectal balloon required
to elicit the reflex was less than the volume required
for the perception of rectal distension, in patients
with faecal incontinence. They also demonstrated
an impaired rectal sensory threshold in these patients, compared to controls. Their conclusion was
that this sensory abnormality and the relatively low
volume required to elicit sphincter relaxation were
conducive to faecal incontinence. However, this
combination of a normally induced distension reflex and impaired rectal sensation is seen in other
conditions such as severe constipation [2].
It is my experience that the volume required to
elicit internal anal sphincter relaxation is lower
than the 25 ml distension reflex threshold in most
subjects, including normal continent individuals.
Hancke and Schurholz's data would support this,
as the mean volume to elicit sensation was 40 ml of
water compared to a 25 ml sensory threshold in the
control group. In addition, the volume required to
elicit the reflex was not significantly different for
the two groups. Although acute rectal distension
elicits this reflex, it is not necessarily the mechanism
which operates in life. The sphincter does not automatically relax with the rectal instillation of fluid
or barium. The distension with faeces may occur
slowly, or more likely the normal activation for
sphincter relaxation is the intramural peristaltic response of the distal bowel during defaecation. Certainly the reflex can be induced electrically by an
electrode in the rectum [3].
Rectal sensation has been shown to be impaired

not only in patients with incontinence, but also in
elderly subjects with faecal impaction [4] and young
women with severe idiopathic constipation [2, 5].
The impaired sensation may therefore reflect a neuropathy which does not necessarily contribute to
the soiling.
Faecal incontinence is likely to be due to a complex combination of abnormalities, including denervation of the pelvic striated musculature, possibly due to pelvic nerve stretching [6], as well as
internal sphincter degeneration [7]. Hancke and
Schurholz have not demonstrated that the sensory
disturbance or an inappropriate inhibitory reflex
contribute or are responsible.
Yours faithfully,
Dr. Michael Kamm
St. Mark's Hospital
City Road
London EC1V 2PS
UK
References
1. Hancke E, Schurholz M (1987) Impaired rectal sensation in
idiopathic faecal incontinence. Int J Colorect Dis 2:146 148
2. Reid NW, Timms JM, Barfield LJ, Donnelly TC, Bannister
JJ (1986) Impairment of defaecation in young women with
severe constipation. Gastroenterology 90:53 60
3. Nagasaki A, Ikeda K, Suita S, Sumitomo K (1984) Induction
of the rectoanal reflex by electrical stimulation. A diagnostic
aid for Hirschsprung's disease. Dis Col Rectum 27:598-601
4. Reid NW, Abouzekry L, Reid MG, Howell P, Ottewell D,
Donnelly TC (1985) Anorectal function in elderly patients
with faecal impaction. Gastroenterology 89:959-966
5. Kamm MA, L~'nnard-Jones JE (1988) Evidence for a rectal
sensory neuropathy in severe slow transit constipation. Gastroenterology 94:A214
6. Snooks SJ, Barnes PRH, Swash M (1984) Damage to the
innervation of the voluntary anal and periurethral sphincter
musculature in incontinence; an electrophysiological study. J
Neurol Neurosurg Psychiatry 47:1269 1273
7. Lubowski DZ, Nicholls RJ, Burleigh DE, Swash M (1987)
Internal anal sphincter damage in neurogenic faecal incontinence. Dig Dis Sci 32:919
233
Response from the author

Idiopathic faecal incontinence - a combination of disturbances
of both sphincter motor response and anorectal sensation
Dear Sir,
The objection of Dr. Kamm that the combination
of a normally induced distension reflex and impaired rectal sensation is not only seen in patients
with idiopathic faecal incontinence but also in
other conditions such as severe constipation does
not contradict the conclusion that impaired rectal
sensation is the cause of incontinence in these patients.
As has been shown by our study, these patients
have both impaired anorectal sensation and reduced squeeze and stress pressures compared to the
matched controls.
Our conclusion was that it is not only the high
sensory threshold, as Dr. Kamm pointed out, but
in fact a combination of these sensory and motor
disturbances that contributes to faecal incontinence.
A high sensory threshold prevents early sensation of rectal movements. The expulsion of the
faeces cannot be controlled by squeezing because of
the inadequate motor response of the voluntary

sphincter of these patients. Thus a combined sensory and motor defect contributes to the soiling of
patients with idiopathic faecal incontinence.
If it is only the rectal sensation that is impaired
and the voluntary sphincter remains normal as in
constipated patients, soiling does not result from
high sensory threshold but impaction does.
The anorectal distension reflex, which independent from sensory impairment is conducted via the
intramural intestinal pathway, was not affected in
our patients with idiopathic faecal incontinence nor
in the controls as is the case in patients with constipation.
Yours faithfully,
Priv. Doz. Dr. E. Hancke
Chirurgische Universit/itsklinik
Klinikum GroBhadern
Marchioninistrasse 15
D-8000 Miinchen 70
FRG
Book review
G. Antes, F. Eggemann: Small Bowel Radiology. Introduction
and Atlas. Berlin Heidelberg New York, Springer 1988. 207 pp.,
276 Figs., (ISBN 3-540-15263-6), Hardcover, D M 190.-.
The current trend for the radiological examination of small
bowel still favours the small bowel enema with duodenal intubation. This atlas, some 200 pages in length with 276 illustrations,
is based on the authors' experience of over 5,000 such intubation
studies. Proponents of the small bowel enema, or enteroclysis,
fall into two camps using either a dilute barium suspension as
advocated by Sellink, or the Herlinger methylcellulose system.
The authors have used both but stipulate a preference for the
methylcellulose technique. I note that there is no mention of the
after effects of methylcellulose, which produces quite severe
diarrhoea. The claim that it produces a "double contrast" picture somewhat overstates the increased transradiancy effect.
This is very attractive and clear in normal proximal bowel, but
is not so evident in distal diseased bowel where greater mixing
between the contrast and methylcellulose just produces a more
dilute single contrast effect. I think this is evident in many of the
illustrations. The techniques, indications and radiological interpretation of the examination are discussed in the first section of
the book. The second part forms the atlas of small bowel diseases with an outline of the clinico-pathological presentation
and radiographic features to accompany the radiographs. All
the references are at the end, and provide an up-to-date summation of the body of literature on this subject. The illustrations are
of good quality and demonstrate adequately the described pathologies. There is an interesting section on motility disorders as
judged from alteration in transit and peristaltic pattern. These
changes seem rather non-specific for reliable diagnosis except in
more gross examples, but this is an interesting observation that
the authors are right to emphasize, though more research is
needed to clarify just how meaningful these changes are. The
value of compression is mentioned though not emphasized perhaps as much as it should be, as without its use lesions will still
be missed even with the enteroclysis technique. There is only
passing mention of plain films, angiography, CT and US in the
diagnosis of small bowel disease. This, as the illustration on the
cover suggests, is an atlas of enteroclysis of the small bowel. It
is a concise and readable text, and can be recommended for
anyone wishing to embark on this type of examination.
C. I. Bartram (London)
233
Response from the author

Idiopathic faecal incontinence - a combination of disturbances
of both sphincter motor response and anorectal sensation
Dear Sir,
The objection of Dr. Kamm that the combination
of a normally induced distension reflex and impaired rectal sensation is not only seen in patients
with idiopathic faecal incontinence but also in
other conditions such as severe constipation does
not contradict the conclusion that impaired rectal
sensation is the cause of incontinence in these patients.
As has been shown by our study, these patients
have both impaired anorectal sensation and reduced squeeze and stress pressures compared to the
matched controls.
Our conclusion was that it is not only the high
sensory threshold, as Dr. Kamm pointed out, but
in fact a combination of these sensory and motor
disturbances that contributes to faecal incontinence.
A high sensory threshold prevents early sensation of rectal movements. The expulsion of the
faeces cannot be controlled by squeezing because of
the inadequate motor response of the voluntary

sphincter of these patients. Thus a combined sensory and motor defect contributes to the soiling of
patients with idiopathic faecal incontinence.
If it is only the rectal sensation that is impaired
and the voluntary sphincter remains normal as in
constipated patients, soiling does not result from
high sensory threshold but impaction does.
The anorectal distension reflex, which independent from sensory impairment is conducted via the
intramural intestinal pathway, was not affected in
our patients with idiopathic faecal incontinence nor
in the controls as is the case in patients with constipation.
Yours faithfully,
Priv. Doz. Dr. E. Hancke
Chirurgische Universit/itsklinik
Klinikum GroBhadern
Marchioninistrasse 15
D-8000 Miinchen 70
FRG
Book review
G. Antes, F. Eggemann: Small Bowel Radiology. Introduction
and Atlas. Berlin Heidelberg New York, Springer 1988. 207 pp.,
276 Figs., (ISBN 3-540-15263-6), Hardcover, D M 190.-.
The current trend for the radiological examination of small
bowel still favours the small bowel enema with duodenal intubation. This atlas, some 200 pages in length with 276 illustrations,
is based on the authors' experience of over 5,000 such intubation
studies. Proponents of the small bowel enema, or enteroclysis,
fall into two camps using either a dilute barium suspension as
advocated by Sellink, or the Herlinger methylcellulose system.
The authors have used both but stipulate a preference for the
methylcellulose technique. I note that there is no mention of the
after effects of methylcellulose, which produces quite severe
diarrhoea. The claim that it produces a "double contrast" picture somewhat overstates the increased transradiancy effect.
This is very attractive and clear in normal proximal bowel, but
is not so evident in distal diseased bowel where greater mixing
between the contrast and methylcellulose just produces a more
dilute single contrast effect. I think this is evident in many of the
illustrations. The techniques, indications and radiological interpretation of the examination are discussed in the first section of
the book. The second part forms the atlas of small bowel diseases with an outline of the clinico-pathological presentation
and radiographic features to accompany the radiographs. All
the references are at the end, and provide an up-to-date summation of the body of literature on this subject. The illustrations are
of good quality and demonstrate adequately the described pathologies. There is an interesting section on motility disorders as
judged from alteration in transit and peristaltic pattern. These
changes seem rather non-specific for reliable diagnosis except in
more gross examples, but this is an interesting observation that
the authors are right to emphasize, though more research is
needed to clarify just how meaningful these changes are. The
value of compression is mentioned though not emphasized perhaps as much as it should be, as without its use lesions will still
be missed even with the enteroclysis technique. There is only
passing mention of plain films, angiography, CT and US in the
diagnosis of small bowel disease. This, as the illustration on the
cover suggests, is an atlas of enteroclysis of the small bowel. It
is a concise and readable text, and can be recommended for
anyone wishing to embark on this type of examination.
C. I. Bartram (London)
Answers:
1. Normal mucosa, lVlUltlple smoom tllnng aetects, tan cmser mspecuon ot me margmm nmng aetects,
concomitant associated mural gas is seen. 2. In the presence of normal mucosa and filling defects due to
intramural gas, there is no differential diagnosis. This is pneumatosis cystoides intestinalis. 3. Chest X-ray.
Pneumatosis cystoides intestinalis occurs most commonly in association with chronic obstructive airways
disease and it is thought that gas "tracks" via the mediastinum to the retroperitoneum and thence into the
mesentery (anatomical theory). 4. Very occasionally pneumatosis is noted in assocation with a carcinoma.
It is thought that carcinomatous necrosis extends into the wall of the bowel and intraluminal pressure
forces air into the sub-mucosal space (mechanical theory).
Lemou!a~13o ql!A~ o!qsuo!lgl0J 0ql s! lgq3A

Ls!souffe!p oql qs!I
-qmso dlo q plnoA~ qdg2ffoIpe~ 2oqlo leq3A
/,asneo lSO!lO)l!I
oql OlglS pue sIsouge!p lg!luoJoJJ!p oql lS!~I
'soougJeoddg IeO!8OlO!peJ oql oq!JasoG
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oql ol gu!J.Iojoz ol .m!.Id poao~sug oq ol suo!lsonb IIV - "fl'N) "pmsonba.~ se~a emouo tun!.leq V "POl!o!IO
sg~ opos!do ~gl.tm!s /:ue j o g~ols!q/:IlmgJ ao l'gUOS.tod snotAo~d o N "u.n3d [gu.ttuopq'e .m 1.tq3~q lo~oq m
o~ugtIO ou sg~ oiOtLL "~uipooiq [gloo.I po.t lq~!aq j o opos!da ue ql!~ pmuoso~d u-gtUOllUO~ plo-~eog-g# S!tLL
AaO}S!H
Ill
Col6i'eclal
Disease
Int J Colorect Dis (1988) 3:235
Acknowledgement to Referees
The Editors wish to express their thanks to the referees of papers.
Their time and trouble is much appreciated.
E. Akovbiantz, Zurich
S. Alexander, London
J. Alexander-Williams, Birmingham
R. E. Allan, Birmingham
T. Allen-Mersh, London
M. Allison, Glasgow
N. Armitage, Nottingham
S. Arnott, London
W. Atkin, London
A. T. R. Axon, Leeds
D. C. C. Bartolo, Bristol
R. W. Beart, Rochester, Minn.
R. H. L. Begent, London
P. Belleveau, Montreal
D. Burleigh, London
H. J. R. Bussey, London
J. Christiansen, Copenhagen
A. W. Clark, Brighton
Z. Cohen, Toronto
D. Colin-Jones, Portsmouth
J. P. Cruse, London
B. J. Cummings, Toronto
J. H. Cummings, Cambridge
J. Cuzick, London
H. B. Devlin, Stockton-on-Tees
M. F. Dixon, Leeds
R. R. Dozois, Rochester, Minn.
P. Durdey, London
G. Ekelund, Malmo
M. S. Elliot, Cape Town
H. Ellis, London
H. J. Espiner, Bristol
W. G. Everett, Cambridge
S. J. Eykyn, London
P. Fairclough, London
P. Farrands, Winchester
M. J. G. Farthing, London
E. Farthmann, Freiburg
V. Fazio, Cleveland, Ohio
L. P. Fielding, Waterbury, Conn.
P. Finan, Leeds
I. G. Finlay, Glasgow
D. Galloway, Glasgow
W. D. George, Glasgow
G. R. Giles, Leeds
O. J. A. Gilmore, London
R. Glass, Swindon
S. M. Goldberg, Minneapolis, Minn.
A. W. Goode, London
P. H. Gordon, Montreal
R. H. Grace, Wolverhampton
B. D. Hancock, Manchester
C. J. Harocopos, London
P. R. Hawley, London
M. M. Henry, London
P. Hermanek, Erlangen
G. L. Hill, Auckland
M. J. Hill, London
J. Thornton Holmes, Peterborough
L. Hulten, Goteborg
R. H. Hunt, Hamilton, Ontario
M. H. Irving, Salford
B. T. Jackson, London
J. R. Jass, Auckland
D. P. Jewell, Oxford
D. Johnston, Leeds
M. A. Kamm, London
S. Karran, Southampton
M. R. B. Keighley, Birmingham
K. Kelly, Rochester, Minn.
M. G. W. Kettlewell, Oxford
J. D. Kettner, Winnipeg
O. Kronborg, Goteborg
J. H. C. Kuijpers, Nijmegen
R. H. S. Lane, Winchester
F. Lazorthes, Toulouse
D. J. Leaper, Bristol
R. Leicester, Gosport
R. Lendrum, Newcastle-upon-Tyne
J. E. Lennard-Jones, London
A. Lewis, London
D. Z. Lubowski, Sydney
D. McGibbon, London
R. S. McLeod, Toronto
M. R. Madigan, Bishops Stortford
P. H. G. Mahieu, Brussels
C. A. Makin, Liverpool
M. Malafosse, Paris
C. G. Marks, Guildford
M.-C. Marti, Geneva
R. Miller, Bristol
B. C. Morson, London
N. J. McC. Mortensen, Oxford
R. W. Motson, Colchester
T. C. Muir, Glasgow
V. Murday, London
T. Muto, Tokyo
B. Nordlinger, Paris
J. M. A. Northover, London
G. D. Oates, Birmingham
N . S. Painter, London
J. Papillon, Lyons
R. Parc, Paris
T. F. Parks, Belfast
E. Parnaud, Paris
J. H. Pemberton, Rochester, Minn.
F. Penninckx, Leuven
J. Peto, London
J. Pezim, Vancouver
R. K. S. Phillips, London
A. Polglase, Malvern, Vict.
A. V. Pollock, Scarborough
R. E. Pounder, London
A. Price, London
J. Rainey, Edinburgh
N. W. Read, Sheffield
K. R. P. Rutter, Camberley
D. Sachar, New York
J.-C. Sarles, Marseilles
P. Schofield, Manchester
W. Shand, London
D. Sheer, London
N. A. Shepherd, Gloucester
D. B. Silk, London
J. Silman, London
A. J. W. Sim, London
A. Sitges-Creus, Barcelona
J. Slack, London
A. N. Smith, Edinburgh
R. Springall, London
G. W. Stevenson, Hamilton, Ontario
I. Talbot, Leicester
I. Taylor, Southampton
R. Telander, Rochester, Minn.
J. P. S. Thomson, London
W. H. F. Thomson, Gloucester
A. Timothy, London
L. A. Turnberg, Manchester
G. N. J. Tytgat, Amsterdam
J. D. Waye, New York
J. Wellwood, London
C. B. Williams, London
N. S. Williams, London
M. Winkler, Schleswig
B. Wood, Liverpool
C. B. Wood, London
N. A. Wright, London
M. Wunderlich, Vienna
A. W. Wyatt, London

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Coloi'eetal

Int J Colorect Dis (1988) 3:191 194

Perineal descent is often present both in patients

employing a combination of static and dynamic

4Fig. 1. Measurement of pelvic floor position at rest (DR) and at

Table 1. Additional pathology revealed by the defaecography in

incontinence outlet obstruction

Fig. 3. Resting pelvic floor position

as the distance in cm of the an 9

The resting pelvic floor position in relation to the

nificantly greater in women with outlet obstruction

incontinence outlet obstruction

Fig. 5. Descent of the pelvic floor during straining (Ds_R) in

Table 2. Pelvic floor position at rest (DR) and during straining

Table 3. Pelvic floor position at rest (DR) and during straining

(Ds_R) in 8 female patients with outlet obstruction

Defaecography with the technique used in this

Int J Colorect Dis (1988) 3:195-200

Rectal cancer: factors influencing the development

Abstract. The study was designed to select criteria

Low anterior resection with or without special

even in the presence of low rectal tumours prompts

Fig. 1. Probability of remaining free of local recurrence after

The analysis of interdependence between pairs of

YEARS AFTER RADICAL A.R,

Fig. 2. Probability of remaining free of local recurrence after

YEARS AFTER RADICAL A.R.

Fig. 3. Probability of remaining free of local recurrence after

Fig. 5. Probability of remaining free of local recurrence after

Table 1. Prognostic factors for the development of local recur-

Fig. 4. Probability of remaining free of local recurrence after

tion and, in the presence of venous or lymphatic

changed over the last decades. At our clinic the local

reappraised. Originally, the necessity for a wide

23. Wenzl E, Wunderlich M, Herbst F, Schemper M, Fell W,

Int J Colorect Dis (1988) 3:201-203

Gastric carcinoma and familial adenomatous polyposis (FAP)

Abstract. We report two cases of FAP associated

A familial type of multiple colonic adenomatous

of 26 studied with FAP. They termed these polyps

Fig. 1. There is a partially ulcerated fungating tumour in the

Fig. 2. Hyperplastic 'fundic gland

Fig. 3. A Fundic gland polyp showing adenomatous dysplasia (boxed

termed 'fundic gland polyps' by Watanabe et al. (Fig. 2). Many

carcinoma. The presence of the polyps increases the

1. Cripps HW (1882) Two cases of disseminated polyps of the

Int J Colorect Dis (1988) 3 : 2 0 4 - 2 0 6

Intraoperative irrigation and primary resection for obstructing lesions

Abstract. The treatment of choice for left sided

The surgical treatment of obstructive lesions of the

Patients and methods

Carcinoma of the left colon, 21 cases

after reduction of the volvulus, the irrigation tube was inserted

The time taken for intraoperative irrigation was

Fig. 3. Antegrade irrigation

Acknowledgements. The authors would like to thank Dr. T.

and in the present study of intraoperative irrigation

Yamamoto and Dr. H. Shida at Tokyo Koseinenkin Hospital

H e used a specially designed irrigation tube which

1. Irvin TT, Goligher JC (1973) Aetiology of disruption of

Int J Colorect Dis (1988) 3:207-209

Function of the striated anal sphincter during straining

Abstract. T h e function o f the striated anal sphincter during d e f a e c a t i o n straining was r e c o r d e d by

Patients with chronic c o n s t i p a t i o n m a y be divided