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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1443_Библиотеки_им_академика_М_И_Перельмана.pdf
x
15 Benign Disease, Fissures, Presentation
and Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197
Mark T.C. Wong and Francis Seow-Choen
16 Chronic Anal Fissure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Siraj Rajaratnam and Ian Lindsey
17 Anal Sepsis: Anatomy, Pathophysiology and Presentation . . . 221
Stanley M. Goldberg and Patrick S. Tawadros
18 Imaging of Anal Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
Steve Halligan and Stuart A. Taylor
19 Management of Anorectal Sepsis . . . . . . . . . . . . . . . . . . . . . . . . 243
Toby M. Hammond and Peter J. Lunniss
20 Perianal Skin Conditions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253
Tamzin Cuming, Angela C. Bailey,
and Parameswaran N. Sashidharan
21 Pruritus Ani . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275
Tim Brown
22 Reconstruction of the Anus and Perianal Region . . . . . . . . . . . 283
David Ross and Marlese Dempsey
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297
Contents
xi
Mostafa Abdel-Halim , MBBCh, MRCS, MSc, MD Department of GI
Physiology , University College London Hospital , London , UK
Angela C. Bailey , BM, BCh, MRCP (UK) Jefferiss Wing
Department of GU Medicine and HIV , Imperial College Healthcare
NHS Trust, St. Mary’s Hospital , London , UK
Paul Boulos , MS, FRCS Department of Surgery ,
University College London Hospital , London , UK
Marylise Boutros , MD Division of Colorectal Surgery,
Department of Surgery , Sir Mortimer B. Davis Jewish General Hospital,
McGill University , Montreal , QC , Canada
Tim Brown , FRCS Department of Colorectal Surgery ,
Royal Victoria Hospital , Belfast , Northern Ireland
Emin Carapeti , BSc, MBBS, MD, FRCS (Gen) Department of Surgery ,
Guys and St. Thomas’ NHS Trust , London , UK
Richard Cohen , MD, FRCS Department of GI Surgery ,
University College London Hospitals , London , UK
James Crosbie , MD, FRCSI Department of Surgery ,
University College London Hospital , London , UK
Tamzin Cuming , MBBS, MA (Cantab), FRCS (Eng), MEd
Department of Surgery, Homerton University Hospital , London , UK
Marlese Dempsey , MD FRCS (Plast) Department of Plastic Surgery ,
Royal Free Hospital , London , UK
Anton Emmanuel , BSc, MD, FRCP, FRCP (Ed) GI Physiology Unit,
GI Physiology Department , University College London Hospital ,
London , UK
Ridzuan Farouk , MD, MCh, FRCS Department of Surgery,
Royal Berkshire NHS Trust , Reading, Berkshire , UK
Contributors
xii
Stanley M. Goldberg , MD, FACS, HonFRACS (Aust), HonFRCS (Eng),
HonAFC (Fr), HonFRCPS (Glasg), HonFRSM (Eng), HonFPCS (Phil),
HonFRCS (Edin), Honoris Causa (Lleida), HonSAS (Spain),
HonJSS (Japan) Division of Colon and Rectal Surgery,
Department of Surgery , University of Minnesota , Minneapolis , MN , USA
Jonathan Gosling , MBChB, MRCS GI Physiology Unit, GI Physiology
Department , University College London Hospital , London , UK
Sarah W. Grahn , MD Division of Colon and Rectal Surgery,
Department of Surgery , University of Minnesota Medical School ,
Minneapolis , MN , USA
Nigel J. Hall , MB BChir, PhD Department of Paediatric Surgery ,
Great Ormond Street Hospital for Children and UCL Institute
of Child Health , London , UK
Department of Paediatric Surgery , Great Ormond Street Hospital ,
London , UK
Steve Halligan , MBBS, MD, FRCR, FRCP Department of Medical
Imaging , Centre for Medical Imaging, University College Hospital,
University College London , London , UK
Toby M. Hammond , MD, FRCS Department of General Surgery,
Broomfi eld Hospital, Mid Essex Hospital NHS Trust , Chelmsford , UK
Edward M. Kiely , FRCS Department of Paediatric Surgery ,
Great Ormond Street Hospital , London , UK
Mary R. Kwaan , MD, MPH Division of Colon and Rectal Surgery,
Department of Surgery , University of Minnesota Medical School ,
Minneapolis , MN , USA
Ian Lindsey , MBBS, FRACS Department of Colorectal Surgery ,
Oxford Radcliffe Hospitals NHS Trust , Oxford , UK
Antonio Longo , MD European Center of Coloproctology and Pelvic
Diseases , Vienna , Austria
Peter J. Lunniss , BSc, MS, FRCS Department of Colorectal Surgery,
The Homerton Hospital London, St. Bartholomew’s
and The Royal London , London , UK
The Royal London Hospital, Barts Health NHS Trust , London , UK
Robert D. Madoff , MD, FACS Division of Colon and Rectal Surgery,
Department of Surgery , University of Minnesota Medical School ,
Minneapolis , MN , USA
Jonathan McCullough , FRCS Department of Surgery ,
University College London Hospital , London , UK
Ayesha Noorani , MB BChir, MA (Cantab), MRCS
Department of Surgery , Addenbrookes Hospital , Cambridge , UK
Contributors
xiii
Marco Novelli , MB ChB, MSc, PhD, FRCPath Department
of Histopathology , University College Hospital NHS Foundation Trust ,
London , UK
Karen P. Nugent , MA, MS, Med FRCS Department of Surgery ,
University of Southampton , Southampton, Hampshire , UK
Marc C. Osborne , MD Division of Colorectal Surgery,
Department of Surgery , University of Minnesota , Minneapolis , MN , USA
Francesco Prete , FRCS Department of GI Surgery ,
University College London Hospitals , London , UK
Siraj Rajaratnam , FRACS Department of Colorectal Surgery ,
Oxford Radcliffe Hospitals NHS Trust , Oxford , UK
Colorectal Surgery Unit North Shore Hospital , Auckland , New Zealand
Jonathan Randall , FRCS Department of Surgery ,
Royal Berkshire Hospital , Reading, Berkshire , UK
Adolfo Renzi , MD, PhD Department of Colorectal Surgery , Villa delle
Querce Hospital , Naples , Italy
Joan Robert-Yap , MD Proctology and Pelvic Floor Unit ,
University of Geneva Hospital , Geneva , Switzerland
Bruno Roche , MD Proctology and Pelvic Floor Unit ,
University of Geneva Hospital , Geneva , Switzerland
David Ross , MD, FRCS (Plast) Department of Plastic Surgery ,
St. Thomas’ Hospital , London , UK
GKT Cancer Reconstruction Service , Guys & St Thomas’ Hospital ,
London , UK
Ruma Saraswati , MB ChB, FEBP, FRCPath Department of Cellular
Pathology , University College London Hospital NHS Foundation Trust ,
London , UK
Parameswaran N. Sashidharan , BSc, MBBS, DV, MD
(Dermatology & Venereology), MSc (Dermatology), Dip GUM, DFFP
Department of Sexual Health , Homerton University Hospital , London , UK
Alexis M. P. Schizas , BSc, MSc, MD (Res), FRCS (Gen Surg)
Department of Colorectal Surgery , Guy’s and St. Thomas’ Hospitals
NHS Foundation Trust , London , UK
Francis Seow-Choen , MBBS, FRCS ED, FAMS, FRES
Fortis Colorectal Hospital , Singapore , Singapore
Karel Skala , MD Proctology and Pelvic Floor Unit ,
University of Geneva Hospital , Geneva , Switzerland
Michael J. Steward , BMedSci (Hons), MB ChB, MRCP, FRCR
Department of Imaging , The Whittington Hospital , London , UK
Contributors
xiv
Patrick S. Tawadros , MD, PhD, FRCSC Division of Colon
and Rectal Surgery, Department of Surgery , University of Minnesota ,
Minneapolis , MN , USA
Stuart A. Taylor , MBBS, BSc, MD, MRCP, FRCR
Department of Medical Imaging , Centre for Medical Imaging,
University College Hospital, University College London , London , UK
Steven D. Wexner , MD, PhD (Hon), FACS, FRCS, FRCS (Ed)
Department of Colorectal Surgery , Cleveland Clinic Florida ,
Weston , FL , USA
Academic Affairs , Florida Atlantic University College of Medicine ,
Weston , FL , USA
Clinical Education , Florida International University College of Medicine ,
University Park , FL , USA
Andrew B. Williams , BSc, MBBS, MS, FRCS Department of General
Surgery , Guy’s and St. Thomas’ Hospitals NHS Foundation Trust ,
London , UK
Alastair Windsor , MD, FRCS (Lon, Ed, Glas) Department of GI Surgery ,
University College London Hospitals , London , UK
Mark T. C. Wong , MBBS (Singapore), FRCS (Edinburgh) Department
of Colorectal Surgery , Singapore General Hospital , Singapore , Singapore
Guillaume Zufferey , MD Proctology and Pelvic Floor Unit ,
University of Geneva Hospital , Geneva , Switzerland
Contributors
1
R. Cohen, A. Windsor (eds.), Anus,
DOI 10.1007/978-1-84882-091-3_1, © Springer-Verlag London 2014
Anal Canal Anatomy and Histology
The anal canal begins at the anorectal junction as
the rectum passes through the pelvic cavity at the
cranial end of the levator ani muscle forming a
sharp angle. The anal canal in adults is between
2.5 and 5 cm in length extending caudally to ter-
minate at the anal verge [ 1 ].
The anal canal is derived from the caudal
hindgut which is divided by the urorectal (cloa-
cal) septum into the urogenital sinus (giving rise
to the urethra and bladder) and rectum [ 2 ]. The
rectum and superior anal canal are separated
from the outside by the anal membrane which
breaks down by the end of the eighth week of
gestation. Abnormal separation of the cloaca,
with the anal canal posteriorly and the urethra
and bladder anteriorly, results in a variety of ano-
rectal malformations. An abnormality in the
development of the urorectal septum in a poste-
rior direction leads to the majority of the anorec-
tal abnormalities such as rectal atresia and fi stulas
between the rectum and urethra, urinary bladder
or vagina.
The anal canal epithelium provides the transi-
tion point between the proximal rectal intestinal
columnar epithelium to the distal stratifi ed epi-
thelium of the skin.
The rectum has a thick muscularis propria layer,
containing an inner circular and outer longitudinal
muscle layer of rectal muscle, which is capable of
peristaltic activity. The muscularis mucosa is also
a prominent feature of the rectum producing a
rhythmic contraction which prevents clogging of
the glands and enhances expulsion of mucus. The
rectal epithelium has numerous mucus-secreting
goblet cells that lubricate the stool and absorptive
cells to absorb water from the stool which are
arranged in closely packed tubular glands, greatly
increasing surface area.
The anal canal epithelium is divided in to
three sections. The proximal canal (cranial end of
puborectalis to the cranial end of the dentate line)
is lined by simple columnar epithelium. The epi-
thelium in the proximal section is similar to that
of the rectum but has shorter more irregular
crypts and more smooth muscle fi bres in the lam-
ina propria layer. This changes to stratifi ed squa-
mous epithelium lower in the anal canal along an
intermediate transition zone just above the den-
tate line [ 3 ]. The transition zone epithelium (zone
between uninterrupted columnar mucosa above
and uninterrupted squamous epithelium below)
has a variable length of between 3 and 11 mm. In
the fetus and newborn, there is a sharp transition,
but in the adult this transition is not so sharp and
stratifi ed squamous epithelium may be present
on columns. The transitional zone epithelium
A. M. P. Schizas , BSc, MSc, MD (Res),
FRCS (Gen Surg) (*)
Department of Colorectal Surgery , Guy’s and St.
Thomas’s Hospitals NHS Foundation Trust ,
London , UK
A. B. Williams , BSc, MBBS, MS, FRCS
Department of General Surgery , Guy’s and St.
Thomas’ Hospitals NHS Foundation Trust ,
London , UK
1
The Normal Anus
Alexis M. P. Schizas and Andrew B. Williams
2
produces minimal mucin and may have features
of squamous epithelium but contains anal glands
and endocrine cells in the submucosal layer. The
distal zone (caudal end of the dentate line to the
anal verge) contains non-keratinizing squamous
epithelium. The epithelium at this level does not
contain glands or hair follicles. The squamous
epithelium of the anal canal merges with perianal
skin (with keratin, hair follicles and apocrine
glands) at anal verge.
The dentate (pectinate) line is at the transi-
tional zone and identifi ed at the caudal end of the
anal valves where they form to create a circum-
ferential line. The anal mucosa forms between
fi ve and ten anal columns (columns of Morgagni)
cranial to the dentate line. The columns are sepa-
rated by anal valves which are easily identifi able
in children but are more diffi cult to identify in
adults [ 2 ]. The anal valves contain the rectal
venous plexus. The anal glands discharge via the
anal crypts at the level of the dentate line. The
anal crypts are not present below the dentate line.
The layer deep to the anal mucosa is formed
by subepithelial tissue, which is composed of
connective tissue and smooth muscle [ 1 ]. Anal
(vascular) cushions are a normal structure of anal
canal, found within this subepithelial layer; these
contribute to anal closure. The cushions contain
blood vessels, connective tissue and smooth
muscle. The anal cushions are thought to be
important in the maintenance of continence and
increase in thickness throughout life.
Beneath the subepithelial layer, the caudal
continuation of the circular smooth muscle of the
rectum thickens to form the internal anal sphinc-
ter [ 3 ]. The internal anal sphincter begins as the
circular smooth muscle passes through the cra-
nial end of puborectalis and terminates caudally
in a clearly defi ned edge at a variable distance
from the anal verge.
The continuation of the longitudinal muscle
layer of the rectum forms the longitudinal muscle
layer in the anal canal and lies between the inter-
nal and external anal sphincters in the intersphinc-
teric space. The anal glands that open via the anal
crypts along the dentate line are found in the inter-
sphincteric space. The longitudinal muscle com-
prises smooth muscle cells from the outer layer of
the rectal wall and striated muscle from levator
ani, puborectalis and pubococcygeus. Caudally
the fi bres from this layer pass through the external
anal sphincter forming septa that insert into the
skin of the lower anal canal and adjacent perineum
as the corrugator cutis ani muscle, giving the
radial corrugation of perianal skin.
The external anal sphincter is made up of stri-
ated muscle and surrounds the longitudinal mus-
cle forming the outer border of the intersphincteric
space. Figure 1.1 shows a sagittal view of the anal
canal. The widely held opinion is that the external
anal sphincter is a tripartite structure [ 4 ]. In this
arrangement the external sphincter is divided into
deep, superfi cial and subcutaneous parts. The
deep section of the external anal sphincter is
fused with puborectalis, with the deep and subcu-
taneous parts of the sphincter forming rings of
muscle, between them elliptical fi bres from the
superfi cial part of the external anal sphincter run
anteriorly from the perineal body to the coccyx
posteriorly. Other models of the external anal
sphincter describe it as a single muscle continu-
ous with the puborectalis muscle [ 3 ], or one that
has a two-part structure [ 5 ]. The two-part model
suggested a deep external anal sphincter and a
superfi cial external anal sphincter. The two-part
model corresponds to the puborectalis and deep
external anal sphincter combined and the fused
superfi cial and subcutaneous sphincter of the tri-
partite model. The external anal sphincter muscle
may not be complete in certain places, and it has
been suggested that the smooth and skeletal mus-
cles form an intimately integrated anal sphincter
complex.
Imaging of the anal canal using anal endo-
sonography (AES) and magnetic resonance
imaging (MRI) has not completely resolved the
anatomical question regarding the external anal
sphincter. Anal canal imaging in women sug-
gested that the anterior external anal sphincter is
shorter than the posterior and that the lateral
external anal sphincter length was longer than the
anterior/posterior length, whereas a more cylin-
drical uniform shape was present in males. It is
however more likely that the women simply have
a shorter external anal sphincter than males and it
does not actually differ in confi guration [ 6 ].
A.M.P. Schizas and A.B. Williams
3
The external anal sphincter is innervated by
the pudendal nerve (S2–S4) [ 1 ], which leaves the
pelvis via the lower part of the greater sciatic
notch, where it passes under the lower border of
the piriformis muscle. It then crosses the ischial
spine and sacrospinous ligament to enter the
ischioanal fossa through the lesser sciatic notch
or foramen via the pudendal (or Alcock’s) canal.
The pudendal nerve has two branches: the
inferior rectal nerve (mainly S2 and S3), which
supplies the external anal sphincter and sensation
to the perianal skin, and the perineal nerve, which
innervates the anterior perineal muscles together
with the sphincter urethrae and forms the dorsal
nerve of the clitoris/penis. In monkeys there is a
degree of cross-innervation between the two
sides of the sphincter, although the degree of
overlap in humans is limited. Puborectalis
receives its main innervation from a direct branch
of the fourth sacral nerve root; it may derive some
innervation via the pudendal nerve.
The autonomic supply to the anal canal and
pelvic fl oor comes from two sources. The fi fth
lumbar nerve root sends sympathetic fi bres to the
superior and inferior hypogastric plexuses, and
the parasympathetic supply is from the second to
fourth sacral nerve roots via the nervi erigentes
[ 1 ]. Fibres of both systems pass obliquely across
the lateral surface of the lower rectum to reach
the region of the perineal body. The internal anal
sphincter has an intrinsic nerve supply from the
myenteric plexus together with an additional sup-
ply from both the sympathetic and parasympa-
thetic nervous systems.
The blood supply to the anal canal cranially, in
keeping with its hind gut origin, is from the supe-
rior rectal artery (branch from the inferior mesen-
teric artery) as its terminal branches pass from
the rectum to the anal canal between the mucosa
and muscle layers. These arteries anastomose
with the middle rectal artery, a branch of the
internal iliac artery. The inferior rectal artery is a
branch from the internal pudendal artery arising
from the lateral wall of the ischioanal fossa,
crossing the fossa to supply the caudal anal canal
muscles and skin. The inferior rectal artery anas-
tomoses with the middle and superior rectal
arteries in the anal canal.
Venous drainage of the anal canal is via the
internal venous plexus in the submucosa and
Anal
columns
Anal
valves
Internal
venous
pexus
Internal anal
sphincter
Intersphincteric
space
Dentate line
Anal verge
Corrugator
cutis ani
Subcutaneous
Superficial
External anal
sphincter
Deep
Puborectalis
Transitional
zone
Fig. 1.1 Sagittal view through the normal anal canal
1 The Normal Anus
4
external plexus outside the muscular layer. The
internal plexus drains mainly to the superior rec-
tal veins and then into the inferior mesenteric
veins. The external and to a lesser extent the
internal plexuses drain into the inferior rectal
vein which drains into the internal pudendal vein.
The internal venous plexus is a site of a portoca-
val venous anastomosis which may lead to vari-
ces in portal hypertension.
The lymphatic drainage of the cranial anal
canal is via the anorectal then perirectal lymph
nodes to the preaortic lymph nodes. The lym-
phatic drainage to caudal anal canal is to the
internal and common iliac lymph nodes. The
lymphatic drainage of the skin of the anal canal is
to the medial superfi cial inguinal lymph nodes.
Anal Canal Physiology
Anal continence is maintained by the complex
interaction of many different variables. Stool
must be delivered at a suitable rate from the colon
into a compliant rectum of adequate volume. The
consistency of this stool should be appropriate
and accurately sensed by the sampling mecha-
nism. Sphincters should be intact and able to con-
tract adequately to produce pressures suffi cient to
prevent leakage of fl atus, liquid and solid stool.
For effective defaecation there needs to be coor-
dinated relaxation of the striated muscle compo-
nents with an increase in intra-abdominal pressure
to expel the rectal contents. The structure of the
anorectal region should prevent herniation or pro-
lapse of elements of the anal canal and rectum
during defaecation.
As a result of the complex interplay between
the factors involved in continence and faecal
evacuation, a wide range of investigations are
needed for full assessment. A defect in any one
element of the system in isolation is unlikely to
have great functional signifi cance, and so in most
clinical situations, there is more than one contrib-
uting factor.
Anorectal physiological studies alone cannot
separate the different structures of the anal
canal; instead they provide measurements of the
resting and squeeze pressures along the canal.
Between 60 and 85 % of resting anal pressure is
attributed to the action of the internal anal
sphincter [ 7 ]. The external anal sphincter and
the puborectalis muscle generate maximal
squeeze pressure [ 8 ]. Symptoms of passive anal
leakage (where the patient is unaware that epi-
sodes are happening) are attributed to internal
sphincter dysfunction, whereas urge symptoms
and frank incontinence of faeces are due to
external sphincter problems.
The function of the internal anal sphincter is
under autonomic control. The sympathetic nerve
supply to the internal anal sphincter is excitatory,
and the parasympathetic supply is inhibitory.
Sympathetic nervous activity is thought to enhance
and parasympathetic activity to reduce internal
sphincter activity. Relaxation of the internal anal
sphincter may be mediated via non- adrenergic,
non-cholinergic nerve activity via the neural trans-
mitter nitric oxide. The internal anal sphincter is
in a state of tonic contraction; as the rectum dis-
tends, to a certain volume, there is refl ex relax-
ation of the internal anal sphincter and followed
by a contraction of the external anal sphincter
(rectoanal inhibitory refl ex).
The rectum, most of the time, is empty as a
result of the angulation at the rectosigmoid junc-
tion. As the volume of faeces increases in the sig-
moid colon, peristalsis forces faeces into the
rectum. The volume required to elicit the rectoanal
inhibitory refl ex correlates with the volume
required for fi rst sensation [ 9 ]. As the rectal wall
distends, afferent signals spread through the
myenteric plexus and initiate a peristaltic wave in
the descending colon, sigmoid colon and rectum.
The internal anal sphincter then relaxes, due to
inhibitory signals from the myenteric plexus, and
contents from the rectum enter the anal canal and
to come in contact with the transition zone mucosa,
allowing discrimination of solid from fl uid and fl a-
tus, a process vital to maintaining continence. In
order to prevent incontinence there is a refl ex con-
traction of the external anal sphincter during this
anorectal sampling process. The rate of recovery
of sphincter tone after this relaxation differs for
the proximal and distal canal, which may be
important in maintaining continence [ 10 ]. In
patients with Hirschsprung’s disease, progressive
A.M.P. Schizas and A.B. Williams
5
systemic sclerosis, Chagas disease and initially
after a coloanal anastomosis, there is no refl ex
relaxation of the internal anal sphincter. Further
studies investigating the role of the rectoanal
inhibitory refl ex have shown that there is a greater
sphincter relaxation of the anal sphincters in
incontinent patients as rectal volume increases and
patients with defaecatory diffi culties have a greater
recovery velocity of the resting anal pressure in
the proximal anal canal [ 9 ].
The rectal defaecatory refl ex described above
is weak and is fortifi ed by the parasympathetic
defaecatory refl ex in order to perform effective
defaecation. The parasympathetic refl ex involves
the sacral segment of the spinal cord. The nerve
endings in the rectum transmit signals to the spi-
nal cord when stimulated. There is then a refl ex
stimulation to the descending colon, sigmoid
colon and rectum via the parasympathetic nerve
fi bres in the pelvic nerves. The parasympathetic
signals intensify the peristaltic wave and relax
the internal anal sphincter. The combined para-
sympathetic and sympathetic refl exes can some-
times effectively empty the left side of the colon
in one movement. In patients following spinal
injury, the refl ex may still be present and
accounts for the involuntary evacuation seen in
these patients.
Defaecation is voluntarily inhibited by con-
traction of puborectalis and the external anal
sphincter; this allows defaecation to be deferred
to a more convenient time. Voluntary defaecation
is initiated by relaxing puborectalis and the
external anal sphincter and contracting the
abdominal muscles. Defaecation is best per-
formed in the squat position (knees higher than
hips, with the back straight and elbows on knees),
allowing the anorectal angle to straighten aiding
defaecation.
The gastrocolic refl ex is another important
refl ex in the timing of defaecation. As the stom-
ach distends, there is an initiation of rectal con-
traction and a desire to defaecate. The exact
mechanism is uncertain but may be due to the
effects of gastrin on the colon. In children this
refl ex is dominant and defaecation follows meals,
whereas in adults cultural factors and individual
habits determine when defaecation occurs.
Normal defaecatory patterns vary consider-
ably between individuals with some opening their
bowels 3 times a day and others every 3 days.
No standardisation exists for either the equip-
ment or technique used for anal canal physiology.
A variety of different systems have been used,
and it is important to note that measurements dif-
fer depending on the system employed. Available
systems include microballoons fi lled with air or
water, microtransducers and water-perfused cath-
eters. These systems may be hand-held or auto-
mated. Hand-held systems are withdrawn in a
measured stepwise fashion with recordings made
after each step (usually of 5–10 mm intervals), or
a single measurement is recorded at the point of
maximum rest or squeeze anal canal pressure.
The automated systems withdraw the catheter at
set rates and allow continuous data recording
(usually at 1 mm intervals).
Each method has been validated for its repeat-
ability and reproducibility, although individual
methods are not interchangeable. The correlation
between measurements made using different sys-
tems and catheters is good; the absolute values are
different, and so when comparing the results of dif-
ferent studies, it is essential to consider the method
used to obtain the pressure measurements [ 11 ].
The majority of anal physiology studies are
performed using water-perfused systems. Water-
perfused catheters use hydraulic capillary infus-
ers to perfuse catheter channels, which are
arranged either radially or obliquely staggered.
Each catheter channel is then linked to a pressure
transducer. Infusion rates of perfusate (sterile
water) vary between 0.25 and 0.5 mL/min per
channel. Systems need to be free from air bub-
bles, which may lead to inaccurate recordings,
and avoid leakage of perfusate onto the perianal
skin, which may lead to falsely high resting pres-
sures due to refl ex external sphincter action.
Perfusion rates should remain constant, because
faster rates are associated with higher resting
pressures, whilst larger diameter catheters lead to
greater recorded pressure.
Vector volume manometry utilises a radially
arranged catheter (eight-channel catheters are
most commonly used) that is withdrawn from the
anal canal during rest and squeeze, and computer
1 The Normal Anus