Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1515_Библиотеки_им_академика_М_И_Перельмана
.pdf
Extraintestinal Manifestations of Inflammatory Bowel Disease 69
increasing doses, reaching a plateau at a dose of
22–25 mg/kg, higher doses are likely to be more effec-
tive than lower doses. A small trial by the Oxford
group using a high dose of UDCA demonstrated sig-
nificant improvement in both the cholangiographic
picture and degree of liver fibrosis but arrived at no
conclusive results on how this treatment affects sur-
vival.
Steroids have been considered potentially useful
for treatment of PSC because of their immunomodu-
latory effect, but no positive impact on the liver dis-
ease has been seen in patients administered cycles of
steroids for their concomitant UC. Steroid therapy
has been evaluated in a number of small, often
uncontrolled, trials. Two such studies on PSC
patients treated with steroids several years ago came
to different conclusions, and another study combin-
ing prednisolone and colchicine therapy failed to
demonstrate any positive effect on disease progres-
sion or survival [67, 68].
Various immunosuppressants have been studied
for the treatment of PSC, most of them with disap-
pointing results. Three trials failed to show any effi-
cacy of methotrexate, alone or in combination with
UDCA [69–71]. Cyclosporine has been found to pre-
vent progression of histological changes in the liver
in the 2-year follow-up of one randomised controlled
trial involving 34 patients. In preliminary studies,
tacrolimus proved capable of improving liver func-
tion test results, but further trials are needed [72].
The outcome of preliminary studies with pentoxi-
fylline and etanercept revealed no clinical benefit
[73, 74].
The course of colitis in patients with PSC is usual-
ly a mild pancolitis. A recent study comparing UC
alone with UC associated with PSC reported a mild
clinical course of colitis in the latter, characterised by
fewer hospital stays and courses of steroid therapy
[75].
The outcome of restorative proctocolectomy in
UC complicated by PSC is not clear. A recent study
compared outcome – in terms of risk of
dysplasia/cancer, morbidity/mortality and long-term
results – of IBD patients with and without PSC
undergoing proctocolectomy. It revealed that IBD
patients with PSC have higher risk of cancer in the
resected colon after proctocolectomy and higher
long-term mortality. Function and quality of life
were similar in the two groups, but the presence of
PSC was associated with worse survival [76].
Fig. 4. Two ERCP images of primary sclerosing cholangitis (our experience)
70 G.C. Sturniolo, M. Barollo, R. D’Incà
The risk of colorectal cancer is reportedly higher
(31%) in UC patients with PSC than in those with UC
alone (5%) [77]. Since the original publication by
Broomè et al. [78] in 1992, about 14 studies have
appeared on the risk of colorectal cancer in patients
with PSC. Some of these studies are difficult to inter-
pret because all patients with colitis are cases of pan-
colitis, which is itself an independent risk factor for
colorectal cancer in UC. There is nonetheless general
consensus that patients with UC and associated PSC
have higher risk of dysplasia and should undergo
colonoscopy with multiple biopsies every year. A
recent work has suggested that UDCA may have a
role in preventing colorectal neoplasia because it can
reduce the amount of toxic hydrophobic bile acids
reaching the colon [79]. A small study on 59 PSC
patients undergoing surveillance colonoscopy found
a significantly lower prevalence of colonic dysplasia
in patients taking UDCA. Another, larger study on
120 patients showed a small reduction in the amount
of dysplasia in patients taking UDCA, but this failed
to reach significance. A recent study by Wolf et al.
compared 28 patients who were given UDCA for 6
months with 92 patients who were not, demonstrat-
ing that UDCA did not reduce the risk of developing
cancer and dysplasia but did reduce the mortality
rate [80]. Recent reports have suggested a worse
course of colitis after liver transplantation despite
immunosuppressant treatment, thus encouraging a
more aggressive surgical approach to the manage-
ment of colitis. Haagsma et al. studied 78 patients
with end-stage PSC or autoimmune cirrhosis treated
with liver transplantation and a median follow up of
7.2 years. They found that the cumulative risk for
IBD was 3%, 12% and 20% at 1, 3 and 5 years, respec-
tively, after liver transplantation. Moreover, IBD dis-
ease-free survival was higher in patients taking aza-
thioprine. Pretransplantation IBD and the use of
tacrolimus were independent predictors for IBD after
liver transplantation. Prevalence of IBD after liver
transplantation was found to be affected by the
immunosuppresion used, and azathioprine seems to
have a protective effect [81].
Dealing with PSC is a real challenge, especially
when associated with UC, but more information is
now emerging on the effects of PSC on clinical fea-
tures of UC, and this is helpful in coping with the
high risk of colorectal malignancies in these patients.
References
1. Das KM (1999) Relationship of extraintestinal involve-
ments in inflammatory bowel disease. Dig Dis Sci
44(1):1–13
2. Bernstein CN, Blanchard JF, Rawsthorne P et al (2001)
The prevalence of extraintestinal diseases in inflam-
matory bowel disease: a population-based study. Am J
Gastroenterol 96(4):1116–1122
3. Snook JA, de Silva HJ, Jewell DP (1989) The associa-
tion of autoimmune disorders with inflammatory
bowel disease. Quart J Med 269:835–840
4. Brandtzaeg P, Halstensen TS, Kett K (1992)
Immunopathology of inflammatory bowel disease. In:
MacDermott RP, Stenson WF (eds) Inflammatory
bowel disease, current topics in gastroenterology.
Elsevier, London, pp 95–136
5. Padolsky DK (1991) Inflammatory bowel disease: Part
1. N Engl J Med 325:928–937
6. Sartor RB (1995) Microbial factors in the pathogenesis
of Crohn’s disease, ulcerative colitis and experimental
intestinal inflammation. Inflammatory bowel disease.
In: Kirsner JB, Shorter RJ (eds) Lea & Febiger,
Philadelphia, pp 96–124
7. MacDermott RP, Elson CO (1991) Mucosal immunol-
ogy I. Gastroenterol Clin North Am 20:397–627
8. Breban M, Hammer RE, Richardson JA et al (1993)
Transfer of the inflammatory disease of HLA B27
transgenic rats by bone marrow engraftment. J Exp
Med 178:1607–1616
9. Taurog JD, Richardson JA, Croft JT et al (1994) The
germfree state prevents development of gut and joint
inflammatory disease in HLA-B27 transgenic rats. J
Exp Med 180:2359–2364
10. Mizoguchi A, Mizoguchi E, Chiba C et al (1996)
Cytokine imbalance and autoantibody production in T
cell receptor-a mutant mice with inflammatory bowel
disease. J Exp Med 183:847–856
11. Chapman RW, Cottone M, Selby WS et al (1986)
Serum autoantibodies in ulcerative colitis and primary
sclerosing cholangitis. Gut 27:86–91
12. Tan EM (1991) Autoantibodies in pathology and cell
biology. Cell 67:841–842
13. Satsagi J, Grootscholten C, Holt H et al (1996) Clinical
pattern of familial inflammatory bowel disease. Gut
38:738–741
14. Rump JA, Scholmerich J, Gross V et al (1990) A new
type of perinuclear anti-neutrophil cytoplasmatic
antibody (p-ANCA) in ulcerative colitis but not in
Crohn’s disease. Immunobiology 181:406–413
15. Hoffenberg J, Fidanza S, Sauaia A (1999) Serologic
testing for inflammatory bowel disease. J Pediatr
134:447–452
16. Lawrance IC, Murray K, Hall A et al (2004) A prospec-
tive comparative study of ASCA and pANCA in Chi-
nese and Caucasian IBD patients. Am J Gastroenterol
99:2186–2194
17. Satsagi J, Grootscholten C, Holt H et al (1996) Clinical
pattern of familial inflammatory bowel disease. Gut
38:738–741
18. Seibold F, Slametschka D, Gregor M et al (1992) Neu-
trophil autoantibodies: a genetic marker in primary
sclerosing cholangitis and ulcerative colitis. Gastroen-
terology 107:532–536
19. Greenstein AJ, Janovitz HD, Sachar DB (1976) The
extraintestinal complications of Crohn’s disease and
ulcerative colitis: a study of 700 patients. Medicine
5:401–412
20. Reinshagen M, Von Tirpitz C (2003) Osteoporosis and
Extraintestinal Manifestations of Inflammatory Bowel Disease 71
other extraintestinal symptoms and complications of
inflammatory bowel diseases. Dig Dis 21:138–145
21. Orchard TR (2001) Arthritis associated with inflam-
matory bowel disease. In: Bayless TM, Hanauer SB
(eds) Advanced therapy of inflammatory bowel dis-
ease. Decker, Hamilton, London, pp 279–288
22. Orchard TR, Wordsworth BP, Jewell DP (1998)
Peripheral arthropathies in inflammatory bowel dis-
ease: their articular distribution and natural history.
Gut 42:387–391
23. Punzi L, Podswiadek M, D’Incà R et al (2003) Serum
human cartilage glycoprotein 39 as a marker of arthri-
tis associated with inflammatory bowel disease. Ann
Rheum Dis 62(12):1224–1226
24. De Vos M, De Keyser F, Mielants H et al (1998) Review
article: bone and joint disease in inflammatory bowel
disease. Aliment Pharmacol Ther 12:397–404
25. Podswiadek M, Punzi L, Stramare R et al (2004) The
prevalence of radiographic sacroiliitis in patients
affected by inflammatory bowel disease with inflam-
matory low back pain. Reumatismo 56(2):110–113
26. De Vos M (2004) Review article: joint involvement in
inflammatory bowel disease. Aliment Pharmacol Ther
20[Suppl 4]:36–42
27. Adler G, Reinshagen M (2003) Extraintestinale Mani-
festationen. Z Gastroenterol 41:54–61
28. Sieper J, Braun J (2001) New treatment options in
ankylosing spondylitis: a role for anti-TNFa therapy.
Ann Rheum Dis 60(Suppl 3):58–61
29. Compston JE (1995) Review article: osteoporosis, cor-
ticosteroids and inflammatory bowel disease. Aliment
Pharmachol Ther 9
:237–250
30. Bernstein CN, Leslie WD (2004) Review article: osteo-
porosis and inflammatory bowel disease. Aliment
Pharmacol Ther 19:941–952
31. Schulte C, Dignass AU, Mann K et al (1998) Reduced
bone mineral density and unbalanced bone metabo-
lism in patients with inflammatory bowel disease.
Inflamm Bowel Dis 4(4):268–275
32. Jahnsen J, Falch JA, Aadland E et al (1997) Bone min-
eral density is reduced in patients with Crohn’s disease
but not in patients with ulcerative colitis: a population
based study. Gut 40:313–319
33. Dinca M, Fries W, Luisetto G et al (1999) Evolution of
osteopenia in inflammatory bowel disease. Am J Gas-
troenterol 94(5):1292–1297
34. de Jong DJ, Corstens FH, Mannaerts L et al (2002) Cor-
ticosteroid-induced osteoporosis: does it occur in
patients with Crohn’s disease? Am J Gastroenterol
97(8):2011–2015
35. Dear KL, Compston JE, Hunter JO (2001) Treatments
for Crohn’s disease that minimise steroid doses are
associated with a reduced risk of osteoporosis. Clin
Nutr 20(6):541–546
36. Bernstein CN, Blanchard JF, Metge C (2003) The asso-
ciation between corticosteroid use and development of
fractures among IBD patients in a population-based
database. Am J Gastroenterol 98(8):1797–1801
37. Greenberg G, Feagan B, Martin F et al (1994) Oral
budesonide for the treatment of active Crohn’s dis-
ease. N Engl J Med 331:836–841
38. Manolagas SC, Jilka RL (1995) Bone marrow, cytokine
and bone remodeling. Emerging insights into the
pathophysiology of osteoporosis. N Engl J Med
332(
5):305–311
39. Andreassen H, Rungby J, Dahlerup F et al (1997)
Inflammatory bowel disease and osteoporosis. Scand J
Gastroenterol 32:1247–1255
40. Lichtenstein GR (2003) Evaluation of bone mineral
density in inflammatory bowel disease: current safety
focus. Am J Gastroenterol 98(12):S24–S30
41. Sambrook P, Birmingham J, Kelly P et al (1993) Pre-
vention of corticosteroids osteoporosis: a comparison
of calcium, calcitriol and calcitonin. N Engl J Med
328:1747–1752
42. Bernstein CN, Seeger LL, Anton PA et al (1996) A ran-
domized placebo-controlled trial of calcium supple-
mentation for decreased bone density in corticos-
teroids-using patients with IBD: a pilot study. Aliment
Pharmacol Ther 10:777–786
43. Cranney A, Welch V, Adachi JD et al (2001) Etidronate
for treating and preventing postmenopausal osteo-
porosis. Cochrane Database Syst Rev (4):CD003376
44. Nousari HC, Provost TT, Anhalt GJ (2001) Cutaneous
manifestations of inflammatory bowel disease. In:
Bayless TM, Hanauer SB (eds) Advanced therapy of
inflammatory bowel disease. B.C. Becker, Hamilton,
pp 271–274
45. Tromm A, May D, Almus E et al (2001) Cutaneous
manifestations in inflammatory bowel disease. Z Gas-
troenterol 39:137–144
46. Fleisher M, Rubin S, Levine A et al (2002) Infliximab in
the treatment of refractory erythema nodosum of IBD.
Gastroenterology 122(Suppl 1):A618
47. Bennet ML, Jackson JM, Jorizzo JL et al (2000) Pyoder-
ma Gangrenosum. A comparison of typical and atypi-
cal forms with an emphasis on time to remission. Case
review of 86 patients from 2 institutions. Medicine
79:37–46
48. Wollina V (2002) Clinical management of pyoderma
gangrenosum. Am J Clinical Dermatol
3:14–58
49. Hohenleutner U, Mohr VD, Michel S et al (1997)
Mycophenolate mofetil and cyclosporine treatment
for recalcitrant pyoderma gangrenosum. Lancet
350:1748
50. D’Incà R, Fagiuoli S, Sturniolo GC (1998) Tacrolimus
to treat pyoderma gangrenosum resistant to
cyclosporine. Ann Intern Med 128:783–784
51. Regueiro M, Valentine J, Plevy S et al (2003) Infliximab
for treatment of pyoderma gangrenosum associated
with inflammatory bowel disease. Am J Gastroenterol
98:1824–1826
52. Brooklyn TN, Dunnill GS, Shetty A et al (2005) Inflix-
imab for the treatment of pyoderma gangrenosum: a
randomized, double-blind placebo controlled trial.
Gut (Epub PMID:16188920)
53. Tavarela Veloso F (2004) Review article: skin compli-
cations associated with inflammatory bowel disease.
Aliment Pharmacol Ther 20(Suppl 4):50–53
54. Fujimoto E, Fujimoto N, Kuroda K et al (2004) Leuko-
cytapheresis treatment for pyoderma gangrenosum.
Br J Dermatol 151:1090–1092
55. Soukiasian S, Foster CS, Raizman MB (1994) Treat-
ment strategies for scleritis and uveitis associated with
inflammatory bowel disease. Am J Ophthalmol
118:601–611
72 G.C. Sturniolo, M. Barollo, R. D’Incà
56. Lamers CBHW (1997) Treatment of extraintestinal
complication of ulcerative colitis. Eur J Gastroenterol
Hepatol 9:850–853
57. Bargiggia S, Maconi G, Elli M et al (2003) Sonographic
prevalence of liver steatosis and biliary tract stones in
patients with inflammatory bowel disease: study of 511
subjects at a single center. J Clinical Gastroenterol
36(5):417–420
58. Hutchinson R, Tyrrel PN, Kumar D et al (1994) Patho-
genesis of gallstones in Crohn’s disease: an alternative
explanation. Gut 35(1):94–97
59. Wiesner RH (1994) Current concepts in primary scle-
rosing cholangitis. Mayo Clin Proc 69:969–982
60. Spurkland A, Saarinen S, Boberg KM et al (1999) HLA
class II haplotypes in primary sclerosing cholangitis
patients from five European populations. Tissue Anti-
gens 53:459–69
61. Grant AJ, Lalor PF, Salmi M et al (2002) Homing of
mucosal lymphocytes to the liver in the pathogenesis
of hepatic complications of inflammatory bowel dis-
ease. Lancet 359:150–157
62. Spirli C, Fabris L, Duner E et al (2003) Cytokine-stim-
ulated nitric oxide production inhibits adenyl cyclase
and cAMP-dependent secretion in cholangiocytes.
Gastroenterology 124:737–753
63. Cullen SN, Chapman RW (2005) Review article: cur-
rent management of primary sclerosing cholangitis.
Aliment Pharmacol Ther 21:933–948
64. Beuers U, Spengler U, Kruis W et al (1992) Ursodeoxy-
cholic acid for treatment of primary sclerosing cholan-
gitis: a placebo-controlled trial. Hepathology 16:707–714
65. Stiehl A, Walker S, Sthiel L et al (1994) Effect of
ursodeoxycholic acid on liver and bile duct disease in
primary sclerosing cholangitis. A 3-year pilot study
with a placebo-controlled study period. J Hepatol
20:57–64
66. Mitchell SA, Bansi DS, Hunt N et al (2001) A prelimi-
nary trial of high dose ursodeoxycholic acid in primary
sclerosing cholangitis. Gastroenterology 121:900–907
67. Buurgert SL, Brown BP, Kirkpatrick RB (1984) Positive
corticosteroid response in early primary sclerosing
cholangitis (abstract). Gastroenterology 86:1037(A)
68. Lindor KD, Wiesner RH, Colwell LJ et al (1991) The
combination of prednisone and colchicine in patients
with primary sclerosing cholangitis. Am J Gastroen-
terol 86:57–61
69. Knox TA, Kaplan MM (1991) Treatment of primary
sclerosing cholangitis with oral methotrexate. Am J
Gastroenterol 86:546–552
70. Knox TA, Kaplan MM (1994) A double-blind con-
trolled trial of oral pulse methotrexate therapy in the
treatment of primary sclerosing cholangitis. Gastroen-
terology 106:494–499
71. Lindor KD, Jorgensen RA, Anderson ML et al (1996)
Ursodeoxycholic acid and methotrexate for primary
sclerosing cholangitis: a pilot study. Am J Gastroen-
terol 91:511–515
72. Talwalkar JA, Lindor KD (2005) Primary sclerosing
cholangitis. Inflamm Bowel Disease 11(1):62–72
73. Bharucha AE, Jorgensen R, Lichtman SN et al (2000) A
pilot study of pentoxifylline for the treatment primary
sclerosing cholangitis. Am J Gatroenterol 95:2338–2342
74. Epstein MP, Kaplan MM (2004) A pilot study of etan-
ercept in the treatment primary sclerosing cholangitis.
Dig Dis Sci 49:1–4
75
. Moayyeri A, Daryani NE, Barhami H et al (2005) Clin-
ical course of ulcerative colitis in patients with or with-
out primary sclerosing cholangitis. J Hepatol Gas-
troenterol 20:366–370
76. Gorgun E, Remzi FH, Manilich E et al (2005) Surgical
outcome in patients with primary sclerosing cholangi-
tis undergoing ileal pouch-anal anastomosis: a case
control study. Surgery 138(4):631–637
77. Chambers WM, Warren BF, Jewell DP et al (2005) Cancer
surveillance in ulcerative colitis. Br J Surg 92(8):928–936
78. Broome U, Lindberg G, Lofberg R (1992) Primary scle-
rosing-cholangitis in ulcerative colitis: a risk factor for
the development of dysplasia and DNA aneuploidy?
Gastroenterology 102(6):1877-1880
79. Pardi DS, Loftus EV, Kremers WK et al (2003)
Ursodeoxycholic acid acts as a chemopreventive agent
in patients with ulcerative colitis and primary scleros-
ing cholangitis. Gastroenterology 124:889–893
80. Wolf JM, Rybicki LA, Lashner BA (2005) The impact of
ursodeoxycholic acid on cancer, dysplasia and mortal-
ity in ulcerative colitis patients with primary scleros-
ing cholangitis. Aliment Pharmacol Ther 22:783–788
81. Haagsma EB, Van Den Berg AP, Kleinbeuker JH et al
(2003) Inflammatory bowel disease after liver trans-
plantation: the effect of different immunosuppressive
regimens. Aliment Pharmacol Ther 18(1):33–44
Introduction
Perianal disease is an important and distinguishing
feature of Crohn’s disease (CD). The incidence of
perianal disease in patients with CD varies from 3.8%
to 81% in different series [1, 2]. While perianal
lesions occur more often in patients with colonic dis-
ease than in patients with small intestinal disease [2],
5% of patients with anorectal CD do not have proxi-
mal disease. Clinical features include hypertrophic
skin tags, ulceration (Fig. 1), perianal abscesses and
fistulae (Figs. 2 and 3), fissures, induration and anal
stenosis [3]. A characteristic feature of perianal CD is
that several abnormalities may coexist. Perianal
abscesses occur in 23–62% of patients and are usual-
ly multiple and complex due to deep, cavitating
ulcers that penetrate the anorectal wall [2]. Crohn’s
abscesses may also arise as a result of an infection of
the intersphincteric anal glands. Anorectal fistulae in
CD arise in 6–34% of patients [2]. According to their
relationship with the sphincters [4], fistulae are clas-
sified in intersphincteric, transsphincteric, suprale-
vator, extrasphincteric and submucosal. The Ameri-
can Gastroenterological Association recommended
the division of fistulae into either simple or complex
[5]. A simple fistula is a superficial, intersphincteric
or low transsphincteric fistula, without secondary
tracts, and it is not associated with an abscess. Com-
Perianal Crohn’s Disease: Assessment with Endoanal
Ultrasonography
Giulio Aniello Santoro, Marianne Starck, Luca Campana, Bjørn Fortling
Fig. 1. Large cavitating ulcer in Crohn’s disease
Fig. 2. Complex perianal sepsis in Crohn’s disease with pres-
ence of multiple external fistulous openings
Fig. 3. Large perianal abscess in Crohn’s disease extending
to the anterior perineum
74 G.A. Santoro, M. Starck, L. Campana, B. Fortling
plex fistulae (high transsphincteric, suprasphinc-
teric, or extrasphincteric fistulae, presence of multi-
ple external openings, secondary tracts or large
abscesses) may result from active rectal disease,
which form deep, cavitating ulceration and fistula-
tion. Rectovaginal fistula in CD occurs in 5.2–10% of
patients [2]. In these fistulae, the internal opening
may be present at the dentate line and the external
opening at the fornix or low in the vagina (anovagi-
nal), or the tract passes directly from the rectum to
the vagina.
The diagnosis of perianal CD can be made when
there is a persistent characteristic pathological lesion
in association with the anal canal in a patient known
to have at least two criteria for the diagnosis of the
intestinal CD: clinical, radiological and histological.
Perianal CD can be diagnosed in the absence of obvi-
ous clinical manifestations on intestinal CD, provid-
ing that there are typical perianal lesions showing
histological evidence of granulomata in biopsies
taken from ulcers or abscesses. Perianal CD is often
difficult to treat, and different management modali-
ties (surgery, medical therapy, diet) have been tried
with variable results [6]. Disease activity appears to
be associated with impaired wound healing, but
wounds usually heal normally when the disease is
inactive. Accurate evaluation is crucial for the treat-
ment plan. Physical examination may reveal simple
fistulae with a relatively superficial position; howev-
er, it is unable to identify ischiorectal, pelvirectal and
horseshoeing tracts and most of the internal open-
ings. When disease is active, the anal lesions have a
characteristic swollen, translucent pink or bluish
appearance with obvious ulceration. As disease activ-
ity resolves, oedema disappears, the tissue becomes
opaque and ulcers heal with a fragile layer of epithe-
lium. Inactive lesions may remain clinically signifi-
cant because of the mechanical effects of the fistula
or strictures.
Due to the limitations of conventional fistulogra-
phy and pelvic computed tomography (CT) scanning
[7], endoanal ultrasonography (EAUS) [8, 9] or
pelvic magnetic resonance imaging (MRI) [10, 11]
have been introduced as useful investigative modali-
ties for perianal CD. In the following chapter, equip-
ment, technique, endosonographic anatomy of the
anal canal, accuracy and reliability of EAUS in the
evaluation of perianal abscesses and fistulae in CD
and comparison of EAUS with MRI is discussed.
Equipment
The most widely used EAUS system is the B-K Med-
ical scanner (Pro-Focus 2202, B-K Medical A/S,
Mileparken 34, DK-2730 Herlev, Denmark), with a
hand-held rotating endoprobe type 1850, which gives
a 360° axial view of the rectal wall (Fig. 4) [12]. The
radial probe has a 24-cm metal shaft with a rotating
transducer at its tip. This 8539 transducer has a fre-
quency range from 5 MHz to 10 MHz with a focal
length of 2–5 cm, and a 90° scanning plane and is
rotated at four to six cycles per second to achieve a
radial scan of the anus and surrounding structures.
The end of the probe is covered with a cone made of
sonolucent polymethyl pentene plastic and 1.7 cm in
outer diameter, which is filled with degassed water to
maintain acoustic coupling between the transducer
and the tissue (Fig. 5). It is important to eliminate all
bubbles within the hard anal cone, given that these
may produce artifact and limit overall utility of the
study. The outer walls of this cone are parallel so that
Fig. 4. B-K Medical anorectal probe type 1850
Fig. 5. The end of the probe is covered with a plastic cone
Perianal Crohn’s Disease: Assessment with Endoanal Ultrasonography 75
the probe may be moved within the anal canal with-
out causing any anatomical distortion. In patients
with a stenotic anus, a smaller endoprobe (7 MHz,
type 6005, focal range: 0.5–3 cm) and cone (diameter
0.9 cm) can be used.
Technology progress allows the three-dimension-
al (3-D) reconstruction of two-dimensional (2-D)
images [12]. It is not necessary to use new ultrasound
probes but to connect the ultrasound apparatus to a
computer equipped with a software (BK3Di). Three-
dimensional reconstruction is based on a high num-
ber of parallel transaxial images acquired using a
special colorectal pullback mover (UA0552) with the
B-K Medical ultrasound probe type 1850. The col-
orectal pullback mover is a computer-controlled,
motor-driven device that can be operated at different
levels of resolution. For endoanal application, the
usual setting is 0.2–0.3 mm between adjacent
transaxial images. Scanning the anal canal with these
settings over a pullback distance of 35 mm will typi-
cally yield 175 parallel images. Data from a series of
closely spaced, 2-D images is combined to create a 3-
D volume displayed as a cube. The 3-D image does
not remain fixed; rather, it can be freely rotated, ren-
dered, tilted and sliced to allow the operator to infi-
nitely vary the different section parameters and visu-
alise the lesion at different angles and to get the most
information out of the data. After data is acquired, it
is immediately possible to select coronal
anterior–posterior or posterior–anterior as well as
sagittal right–left views. The multiview function
allows up to six different and specialised views at
once with real-time reconstruction. If one wants to
see the internal structure, a volume representation
may be chosen. In this, one allows the ray to pass
through the data, and contributions from different
depths are added together in some way and used to
construct the image pixel on the screen (volume ren-
dering). “Volume render mode” is a special feature
that successfully can be applied to high-resolution 3-
D data volumes. Imaging processing includes maxi-
mum intensity, minimum intensity and summed
voxel projections, combined with positional or inten-
sity weighting. This technique changes the depth
information of 3-D data volume so information
inside the cube is reconstructed to some extent.
Extensive anorectal examinations, however,
require moving the transducer head. Probe move-
ment can cause artifacts and change anatomical pres-
entation. The new B-K Medical 2050 anorectal trans-
ducer is designed so that no moving parts come into
contact with human tissue (Fig. 6). The transducer’s
360° rotating head, the proximal–distal actuation
mechanism and the electronic mover are fully
enclosed within the housing of the slim probe. Both
3-D data-set acquisition and high-precision position-
ing of the scan head over a longitudinal distance of
60 mm are accomplished at the touch of a button,
allowing information gathering without having to
move the probe’s position. The 2050’s double crystal
covers a frequency range from 6 MHz to 16 MHz.
In females, transvaginal endosonography (TVS)
can be performed in case of anal pain or stenosis or
to obtain additional information using the same radi-
al probes. Moreover, for sagittal and conventional
transverse imaging of the pelvic floor, including
color Doppler, a biplane, high-frequency transducer
with a long linear and transverse array can be used
(B-K Medical 8658 probe) (Fig. 7). Both arrays are
placed at 90° to each other and at 90° to the longitu-
dinal axis. The transducer can be placed resting on
the posterior vaginal wall. With the patient lying on
her back on a table or in a gynecological chair, the
anterior vaginal wall will softly contact the surface of
the ultrasound transducer without disturbing the
functional anatomy.
Fig. 6. B-K Medical anorectal probe type 2050
Fig. 7. B-K Medical linear probe type 8658
76 G.A. Santoro, M. Starck, L. Campana, B. Fortling
Transperineal ultrasound (TPUS) represents
another method by which to detect perianal inflam-
matory disease, which can be performed using regu-
lar convex and linear high-resolution ultrasound
probes [13]. A convex 3.5 -MHz probe provides a
general overview over perianal anatomy, identifying
bladder, rectum, prostate gland and urethra or vagi-
na and uterus. Further investigation is performed
with a 10-MHz linear probe for a much more detailed
imaging of perianal inflammatory disease.
Technique
Endoluminal ultrasound is usually performed with
the patient in the left lateral decubitus position.
Before the probe is inserted into the anus, a digital
rectal examination should be performed. If there is
an anal stenosis, the finger can check to determine
whether it will allow easy passage of the probe. A gel-
containing condom is placed over the probe, and a
thin layer of water-soluble lubricant is placed on the
exterior of the condom. Any air interface will cause a
major interference pattern. The probe is then ready
for insertion through the anal canal. The patient
should be instructed before the examination that no
pain should be experienced. Under no circumstances
should force be used to advance the probe.
When the spigot for introducing water into the
plastic cone is pointing toward the ceiling, by con-
vention, the anterior aspect of the rectum will be
superior (12 o’clock) on the screen, right lateral will
be left (9 o’clock) on the screen, left lateral will be
right (3 o’clock) on the screen and posterior will be
inferior (6 o’clock) on the screen (just as in the image
on axial CT scan). Some adjustments may have to be
made in the gain of the ultrasound unit to provide
optimal imaging. It is always possible to perfectly
depict all layers of the anal canal circumferentially.
This is very important when assessing the canal at
different levels. At the origin of the anal canal, the
“U”- shaped sling of the puborectalis is the main
landmark and should be used for final adjustment
[12]. Once the entire canal down to the anal margin
has been evaluated, the probe is removed. It is not
uncommon to require several passes along the full
length of the anus to gain all the information neces-
sary. In some instances, two to six passes may be
required to properly evaluate a complex perianal
sepsis.
Endosonographic Anatomy of the Anal Canal
Knowledge of the anal canal and pelvic floor anato-
my is required in order to better understand how
perianal sepsis develops and to more accurately clas-
sify fistulae and abscesses. On ultrasound, six hypoe-
choic and hyperechoic layers can be seen in the nor-
mal anal canal [14]. The ultrasonographer must have
a clear understanding of what each of these six lines
represent anatomically. From inner to outer, the first
hyperechoic layer corresponds to the interface of the
plastic cone with the anal mucosal surface, the sec-
ond hypoechoic layer to the mucosa, the third hyper-
echoic layer to the subepithelial tissues, the fourth
hypoechoic layer to the internal anal sphincter (IAS),
the fifth hyperechoic layer to the longitudinal muscle
(LM) and the sixth mixed echogenic layer to the
external anal sphincter (EAS) (Fig. 8). Three-dimen-
sional endorectal ultrasound offers a valuable sup-
plement to conventional ultrasound. The six layers of
Fig. 8. Normal ultrasonographic six-layer structure of the
mid anal canal in a male. Axial image (a), schematic repre-
sentation (b)
a
b
External anal sphincter
Subepithelial tissue
Longitudinal muscle
Internal anal sphincter
Perianal Crohn’s Disease: Assessment with Endoanal Ultrasonography 77
the anal canal are clearly illustrated in the coronal
plane as well as in the transaxial and the longitudinal
image planes (Fig. 9).
The hypoechoic layer that represents the IAS can
be traced superiorly into the circular muscle of the
rectum. Its thickness varies from 1.5 mm to 4 mm
(mean 3.0±0.5 mm) and increases with age owing
the presence of more fibrous tissue as the absolute
amount of muscle decreases. The longitudinal mus-
cle is 2.5±0.6 mm in males and 2.9±0.6 mm in
females. This muscle is moderately echogenic, which
is surprising, as it is mainly smooth muscle; howev-
er, an increased fibrous stroma may account for this.
The average thickness of the EAS is 8.6±1.1 mm in
males and 7.7±1.1 mm in females. Thickness of the
IAS and EAS should be measured at the 3 o’clock
and 6 o’clock positions in the midlevel of the anal
canal.
Ultrasound imaging of the anus can be divided
into three levels: deep, mid and superficial [14]. The
level refers to the following anatomical structures: (1)
deep: the sling of the puborectalis and the deep part
of the EAS; (2) mid: the anococcygeal ligament,
superficial part of the EAS, IAS and perineal body;
and (3) superficial: the subcutaneous part of the EAS.
The first ultrasound image recorded is normally at
puborectalis level, where the perineal body is also
seen in females. This image is normally documented
and labeled HIGH (Fig. 10). In a normal patient,
moving the probe a few millimetres in the distal
direction will show an intact anterior EAS forming
just below the superficial transverse perineal mus-
cles. This image is a mid-canal projection where the
IAS, conjoining longitudinal muscle and the superfi-
cial EAS all are identified. This image will be labeled
MID (Fig. 11). When the probe is pulled further out,
the image of the IAS will disappear and only the
subepithelium and the subcutaneous segment of the
LM + EAS will be seen. This last image will be labeled
LOW (Fig. 12). The anterior part of the EAS differs
between genders. In males, it is symmetrical at all
levels; in females, it is shorter anteriorly and there is
no evidence of anterior ring high in the canal
(Fig. 13). In examining a female subject, the ultra-
sonographic differences between the natural gaps
(hypoechoic areas with smooth, regular edges) and
sphincter ruptures (mixed echogenicity, due to scar-
ring, with irregular edges) occurring at the upper
anterior part of the anal canal must be kept in mind
[15].
Fig. 9. Normal ultrasound anatomy of the sphincter com-
plex in three-dimensional image
a
b
Fig. 10. Normal ultrasound anatomy of the deep level of the
anal canal demonstrating the puborectalis. Anteriorly, a
thin arc of muscle from the deeper part of the sphincter
may be seen in males (a) whereas the deep part of the
external sphincter is not recognisable in females (b)
External anal sphincter
Internal anal sphincter
Longitudinal muscle
78 G.A. Santoro, M. Starck, L. Campana, B. Fortling
Ultrasonographic Assessment of Perianal Crohn’s
Disease
Accurate identification of all loculate purulent areas
and definition of the anatomy of the primary fistu-
lous tract, secondary extensions and internal open-
ing is crucial for the treatment plan. EAUS has been
demonstrated to be a very helpful diagnostic tool in
accurately assessing all fistula or abscess characteris-
tics [8–11, 16, 17]. Ultrasound examination with the
2050 transducer is generally started using 13 MHz,
changing to 12 MHz or 9 MHz to optimise visualisa-
tion of the deeper structures external to the anal
sphincters. The puborectalis muscle and EAS, LM
and IAS should always be identified and used as ref-
erents for the spatial orientation of the fistula or
abscess.
An anal abscess appears as a hypoechoic, disho-
mogeneous area, sometimes with hyperechoic spots
within it, possibly in connection with a fistulous tract
directed through the anal canal lumen. Infection can
spread in a number of directions, usually along the
path of least resistance. Abscesses are classified as
superficial, intersphincteric (Fig. 14), ischiorectal
Fig. 11. Bulbospongiosus muscle, transverse perineal mus-
cles and external anal sphincter meet in the perineal body.
In males (a), a plane of fat persists between the transverse
perinei and the external sphincter whereas in females (b),
the transverse perinei fuse with the external sphincter.
Schematic representation (c)
ba
Fig. 12. Image at the superficial level demonstrating the sub-
cutaneous external anal sphincter. The internal sphincter is
absent at this level
c
Bulbospongiosus
Transverse perineii
Longitudinal layer
Internal anal sphincter
Perineal body
External anal sphincter
Соседние файлы в папке Библиотека им академика М.И. Перельмана