A CLINICO.PATHOLOGICAL STUDY OF ANAL FISTULAE

9ttV 

A CLINICO.PATHOLOGICAL STUDY OF ANAL FISTULAE 

COMPARISON BETWEEN 

SIMPLE VERSUS COMPLEX CASES 

Thesis 

Submitted in partialfulfillment of Master Degree in General Surgery 

By 

Tamer Mohamed Nnbil 

Supervised by 

Fro. Dr. Kaiss Abdel-Dnyem Abul-Ata 

Profe s or of G ene r a I Sur gery 

Faculty oJ'Medicine 

Cairo University 

Dr. Hany Mahamoud Khattab 

Assistant Pro. Of Pathologt 

Faculty af nedicine 


Dr. Hesham Mahmoud Salah Eldin Amcr 

Asistant Pro. of general Surgery 

Faculty of medicine 

Cairo lJniversity 

Faculty of meclicine 


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ABSTRACT 

The abscess-fistula sequence is the accepted hypothesis for pathogerresis ofanal fistulae' 

Anal fistulae may be either simple or complex Anal fistulae'sulgery isnotoriousfor 

omplications of recurence and ittcontinence ' 

Both of these complications may be either related to iatlogenic mishaps or incomplete 

ssessment of the nature and extent of pathological involvement . 

The aim of this work is to assess the role of specific infection especially cytomegalovirus in 

he pathogenesis of anal fistulae' 

The literature on t'he subject is scanty and little has been written about the relationship 

rctrreeru cytomegalovinrs dise$e and anorectll fistrrla€' 

This wor.k was done on Zg patients presenting with anal fistulae in Kasr-El-Aini hospital' 

A pathological study of excised specimens was done to discover prcsence of paftogens 

rsing 

A Hx. and Eosin staining 

B. ftnmuno histochemical staining to detect cytomegalovirus altigens' 

The patients were grouped according to Park's (1976) classificatioD into 

iroup A: lntersphincteric fistrrlae Group B: Transsphincteric fistulae 

24 cases fufiher subdivided into 

5 Cases 

6 cases offissure fistulae 

7 case simple low anal fistulae 

l1 cases of comPlek fistulae 

There was no cases of supra sphincteric or exfta sphincteric fistulae 

Routine histopathological examination using Hx and eosin was negative for detection of 

pecific pathogens . 

, However itnmuno histopathological arrerrm"ni using monoclonal antibOdy for 

;ytornegalovirus antigens has revealed the prcsence of positive'staining in 7 cases. The positive 

*ained cclls were within the squamous epiftelium surrounding the internal opening of the 

:xcised fistulae 

All positive oases were mainly in the patients presenting wiftr intenphincteric fistulae' 

' 

St+$stical analysis revealed statistically significant association of positive cytomegelovirus 

mtigen in patients with low intersphinoteric fistulae especially those with fissure fistulsF. 

This result could be a preliminary report which need firrther verification and reusing severf,l 

;pecrrlations.

To My FamitY 

And Sincere YAHYA 

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ACKNOWLEDGMENT 

I 

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This work was suggested by prof Dr Kaiss Abder-Dayem prof. of 

General surgery, Cairo university and Dr lleslraru Amer Assistant prof. of 

General surgery cairo univelsity to whom I am deeply indebted for their 

continuous supervision, valuable suggestions, unfaiting help. and 

generosity in giving me a lot of their tinre in preparing this work 

The help of Dr Hany Khattab Assista't prof. of pathorogy cairo 

university, in outlining the pathological part of the work ancl supervising 

it is greatly appreciated 

{ 

I wish to thank Dr Abdel-Aziz Kha'ris assisrant prof. of general 

surg,ery cairo ruriversity ancl Dr. nMR Mnssoud Lecturer ofurology 

Cairo university for their effort in prepnring this work. 

il 

I owe special thanks to the staffof rrry surgicardepartrnent and my 

colleagues for their sincere cooperatiorr in preparing this work 

mentioning Moharned El-Marzoky Assistant lecturer of General surgery, 

cairo university for lris help and encouragenrent not only in preparing 

this work but also in rny career in general 

t

CONTENTS 

page 

* 

i 

* 

t 

Part I 

lntroduction and lirn of the work 

Part II Review of literature 

Anatomy 1. 

Dernographic stuch' 

Aetiology 

Pathology 

Incidence 

subdivisions 

Paft III Material and rrrcthocls 

Material 

Methods 

Part IV 

History 

Examinatiorr 

Instrutnentat i, rrt 

Investigation:. 

Operative firi'lirrgs 

Pathological rtur.lv 

Sltort term fullow up 

Results 

Part V 

Discussion 

Part VII 

Surnmary 

References 

fuabic summary 

I 

2 

l7 

l8 

4l 

44 

45 

53 

56 

56 

57 

58 

s9 

6l 

62 

65 

66 

8l 

87 

90

List of Tables 

Table 

Table (l): Clinical Features Suggesting Possible 

Gastrointestinal Cytomegalov irus Disease. 

pfge 

34 

Tab.le (2): Methods Used To Diagnose 

Gastrointestinal Cytomegalovirus Disease. 

35 

Table (3):showing Distribution of cases according to 66 

classification of Fark's for anal tistula. 

Table (4): showing results of laboratory serological studies E7 

in the group under study. 

Table (5): showing the distribution of positive cases 79 

with cytomegalovirus detected in the pathological 

specimen of their fistulae. 

Table (6): showing distribution of,postoperative recurrent 80 

cases within the studied group.

List of Fisure$ 

Figure 

Page 

Fig. (l): Anal canal 3 

Fig. (?): Epithelium lining of the anal canal. 5 

Fig. (3): An anal gland connected to an anal pit. 5 

Fig. (a); The voluntary and involuntary muscles of the anal canal. 

Fig. (5): The levator ani muscles. 

Fig (6): Puborectalis muscle. 

I 

l0 

l0 

Fig. (7): Coronal diagram ofthe para-anal and para rectal space$. 13 

Fig. (8): Lateral diagram ofthe posterior spaces. 13 

Fig. (9): Coronal diagram of the para-rectal 14 

and phra-anal spaces illustrating how an abscess can track 

posteriorly from one lateral.space to gain access to contralateral 

space. 

Fig. (10): Endoscopic gastric mucosal biopsy speciinen' 28 

from an AIDS patient showing typical cytomegalicell shows a 

Iarge, densely stained nucleus with intracytoplasmic inclusions 

(original maginfi cation x400), 

Fig. (l l): Routine histiologic section ftom an AIDS patient. 

3l 

Left, the many cytomegalicells show infection of various cell 

types including vascular endothelium (small arrow), fibroblasts 

(medium arrow), and smooth muscle cells (large anow) 

(original magnification x 200). Right, rnost of endothelial cells 

in the three blood vesselshown arc cl4omegalic. Ischemi as a 

result of vascular occlusion may be important in the 

pathogenesis of ulceration (original magnification x 200).

Fig. (12): Typei of Intersphincteric fistulae. 47 

Fig. (13): Types of Trans-sphincteric fistulae. 50 

Fig. (la): Types of Suprasphincteric fistulae. 

5l 

Fig. (15): Tlpes of Exfrasphincteric fistulae. 52 

Fig. (16): showing fistulography of case 5,showing 68 

high perianal fistula. 

Fig. (l?): showing endo anal sonography of case No 9, with 69 

right Intersphincteric fi stulous track. 

Fig. (18): showing endo anal sonography of case No 10, with 69 

right transsphincteric fi stulous track. 

Fig. (19): showing MRI of the pelvis of case No 28, 70 

with a fistulous track extending from right perianal region to 

posterolateral aspect of the canal below level of pelvic 

diaphragm. 

Fig. (?0): showing a stratified squamous epitelium adjacent to _ 72 

a fistulous tract with mild epitelial hyperplasia with focal 

koilocytosis (H & E x 40). Case No. 14. 

Fig. (21): showing a fistulous tract lined by septic 72 

granulation tissue with few giant cells (H & E x 100). Case No. 

t7. 

Fig. (22): showing high power of the previous case 

73 

with 2 giant cells sunounded by many inflammatory cells (H & 

E x 400). 

Fig. (23): showing another giant cells surrounded by many 73 

inflammatory cells (H& E x 400). Case No. 19.

Fig. (24): showing an imrnunostaining for CMV with negative 

'Is 

staining of the epithelium adjacent to the fistula (pAp x 40). 

' Case No. 16. 

Fig. (25): showing an immunostaining for CMV with positive 75 

staining of the epithelium (PAP x 40). Case No. 17. 

Fig. (26):,showing an immunostaining for CMV with positive 

staining of the epithelium (PAP x 40). Case No. 18. 

T6 

Fig. (?7): showing an immunostaining for CMV with positive 76 

cytoplasmic and nuclear staining of the epithelial cells (pAp x 

100). Case No. 9. 

Fig. (28): showing an immunostaining for CMV with positive 77 

cytoplasmic and nuclear staining of the epithelial cells (pAp x 

400). Case No. 9. 

Fig. (29): showing an immunostaining for CMV wjth positive 77 

cytoplasmic staining of the epithelial cells (PAp x 400). Casd 

No.7. 

Fig. (30): showing an immunostaining for CMV with 78 

positive nuelear staining of the epithelial cells (pAp x 400). 

Case No.23. 

Fig. (31): showing an immunostaining for CMV with 78 

positivr.nuclear staining of the epithelial cells (pAp x 

400).Case No. 26.

Anal Fhtula 

Inlroduction & Ain of Work 

INTRODUCTION 

{t 

The abscess-fistula sequence is the accepted hypothesis for 

pathogenesis of anal fisiulae. 

Anal fisftrlae may be either simple or complex Anal fistulae surgery is 

notorious for complications of recurrenr* und incontinenc e (Keighley, 

Iees). 

fE 

Both of these complications lnay be either related to iatrogenic. 

mishaps or inoomplete assessment of the nature and extent of pathological 

involvement (Keighley,1993)^ 

Binderow and Warner, (1994) stated that abscesses secondary to a 

specific aetiology comprise less than l0% of the total number of cases. 

AIM OF THE WORK 

t 

The aim of this work is to assess the role of specific infection 

especially cytomegalovirus in the pathogenesis of anal fistulae. 

The literature on the subject is scanty and little has been written about 

the relationship betweens cytornegalovirus disease and anorectal fistulae. 

t[

Anal Fbtula 

Rcrtlew of Literamrc 

ANATOMY 

Detailed anatomical knowledge of anal canal is essential for proper 

l* understanding of pathologlcal changes that occur in this area. 

' 

The goal of this chapter is to describe functional anatomy of 

ilroreatum and pelvic floor particulady from point of view of the surgeon 

performing pelvic and anal surgery. 

Anal Cennl: 

- $kin of anal verge below. 

* 

Short canal 3-4 cm long extending from anorectal ring above to hairy 

L Relatisns 

Circurnferentially, surrounded by sphincters keeping it closed at rest 

with opposition of its lateral walls forming antero-posterior slit. 

Posteriorly related to coccyx with fibrofatty muscular tissue in between. 

t 

t 

, Laterally related to ischiorectal fossa containing inferior hemorroidal 

Anteriorly 

trn male 

vessels and pudendal nerve in Alcock's canal. 

Posterior border of bulb of urethra. 

Urogenital diapluagm containing mernbranous urethra. 

In female 

Perineal body and lower part of posterior vaginal wall 

(Goligher et aL, 1955).

AnalFbtula 

Review of Literature 

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Aml iltUo 

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Fie. (l) Anal canal 

II- Epith,elium of anal csnill 

i} 

below. 

Columnar epithelium above the anal valves and squamous epithelium 

il 

The pectinate and dentate lines are synonymous representing site of 

anal valves which are located at junction of middle and distal two thirds of 

internal sPhincter.

Anal Fbtttlr 

Rrr.la* of Ltterawre 

N.B, The valves are remttdnts of pmctodeal membmns whieh seprates 

post allantoic gutfrom proctodean . 

Above each valve is a pit l'3nun in depth (fual cn/pt) connected to 

anal crypts are a variable number of glands (4-I0) traversing submueosa to 

terminate in intersphincteric plane, if obstructed thie will lead to perianal 

abscess and fistula. occasionally 2 glands open in the same crypt. 

f 

Cranial to anal valve the mucosa is throv*n into 8-14 longituclinal 

folds (columns of Morgagni) below which lies internal hemonhoidal 

plexus. Each adjacent 2 columns being connected at pcctinate line on anal 

valve (Goligher, I 984). 

* 

The mucosa aboye pectinate line is lined by severalayers of cuboidal 

cells for '4-l cm from anal valves which gradually changes to single layer 

of colurnnar cells whieh is characteristic of rectal epithelium (I{alls, 1958), 

The color of mucosa changes from deep purple €r,ftending 0.5-lcm 

above dentate line to pink characteristic of rectal mucosa. 

This area above dentate line is ealled anal transitionT-ane (Dathte and 

Bennett, 1963). 

+ 

Caudal to denttfie /ine modified squamous epithelium devoid of hair, 

sebaceous and sweat glands. The lining epithelium is stratified squamous 

with hair and glands at anal verge only. 

*

Anal Fhtula 


I 

It is importanthat none of mucosar boundaries described above are at 

the same lever at ail places around circumference of anar canar (I{ark, 

r958). 

F.clffi 

Mo{il|.{t i$fiffir 

ipllhrlrm 

rill orffil' 

Fig.(Z): Epithelium lining of the anal canal. 

Anrl rlcnrl 

Fig. (3): fur anal gland connected to an analpit.

AnalFbtula 

ReYtew olllterature 

Anel Cannl Musculnture 

The muscles form a hrbe within funnel the side of the funnel are 

levator ani while the stem is E.A.S. (exter,nal anal sphincter). The tube 

inside the stem is tAS (internal anal sphinctet) (McMinn, 1990) * 

I.A.S. 

. Visceral in origin 

r Continuous above with circular muscle coat of the rectum 

. Below ends with well defined rounded edge l-l t/z em below 

dentate line 

. 0.2-0.3mm thick and it surrounds the entire canal 

(Eisenhummer, 1953). 

* 

E.A.S. 

. Somatic in origin. 

r It is an elliptic cylinder muscles' 

r Continuous with puborectali superiorly 

. Inferiorly it becomesubcutaneous Extends lower than I'A.S. 

r Although in fixed specimens E.A.S. extends lower than I'A'S' 

however at opetatior I.A.S. is usually fomd to be lower 

F 

furatomical Texts described 3 parts of E.A.S. which are surgically 

indistinguishable flyaH h, I I 79). 

Subcutaneous part directly below I.A.S. can easily differentiatedue 

to its division by longitudinal muscle fibers into 8'12 bundles. 

*

AnalFbtula 

Review oJ Literature 

rt 

The upper part of E.A.S. comprising the previously described 

superficial and deep parts which can't be differentiated neither by naked 

eye or histologically from each or from puborectalis fibers with which it 

fuses above (Pena, 1987). 

Attachment of E.A.S. 

Fibers of E.A.S. surround the canal are rarely if ever inserted in pubis 

anteriorly or coccyx posteriorly. 

Posteriorly 

Attacheci to 

r $kin superficially 

* 

. r Anococcygeal raphe and coccyx more deeply 

. It is Continuous with puborectalis at anorectal ring. 

Anteriorly 

. Skin superficially 

r Superficial transverse perineal muscle more deeply 

r It hoceeds most deeply with puborectalis towards pubis at 

level of anorectal rins. 

n 

+ 

Longitudinal muscle fibers 

t 

a 

Lie between I.A.S., E.A.S. (Longitudinal conjoint ligament) 

Superiorly continuous with long. muscle of rectal wall and pubo 

coccygeus muscle (Ifiood, 1985). 

. Inferiorly the fibers fall throughsubcutaneous 

part of E.A.S. 

with attachment to perianal skin. 

are called the corrgator cutis ani. 

These dermal terminations

Anal Fbtuh 

Raiev otLiteranre 

Levator ani muscle 

Sheet of muscle fibers which originate from side wall of pelvis. 

r pubic bone in front. 

r Ischial sPine backward. 

. Intervening obturator fascia. 

* 

This sheet fuscs with its fellow forrning a sling constituting part of 

sphincter mechanism. Formed of 3 parts 

r Ischiococcygeus. 

. Pubococcygeus. 

r hrborectalis. 

Iscihococcgeus 

' Origtn 'Iscial spine' - Obtwator fascia' 

r Course 

- Caudally, posteriorly and medially 

. Insertion - S4-5 of sacrum - Anococcygeal raphe' 

il 

Pubococcygeus 

. Origtn - Obturator fascia - Ptrbis' 

r Course 

- Caudally, posteriorly and medially 

r Insertion decussate with fibers from conualatEral side. Its 

medial fibers fuse with perineal body, vagina or prostate 

and form part of longitudinal. Muscle bundle as it traverses 

in intersphincteric Plane 

f 

|}'

Anal Fbtula 


Puborectalis 

a 

. Origin - Pubis. - Fascia of urogenital diaphnagm. 

r Course posteriorly along side of anorectal ring. 

r lnsertion it joins fibers from the other side forming sling 

behind rectum which is an important land mark, its 

incision will lead to fecal incontinence. 

+ 

whether puborectalis and E.A.s. should be considered as one 

anatomic muscle goup is subject of controversy the best evidence that the 

two are of the sarne striated muscle complex is provided by (wendell- 

Smith,I 985)(IVood, I 985). 

CtcuL. nr gla ol rtolrm 

DE6F erl€mel 

Aaorrclrl 

rhg 

hllnn l hfiro.thoHrl 

vrh 

hlcrnel tpltficlor 

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|l 

Conhlned bnfilludhd 

|nulcb 

Suporflclrl .rlernel 

hlt?rwfcultr 

g;oovl 

Co'rruf,|.tor cutb snl 

+ 

Subculrn.ou! arlrrill 

rphhchr,fl'rrcb 

Fig. (a) The voluntary and involuntary muscles of the anal canal.

Anal Fbtula 

R*iew oJLiterature 

Srilrrl 

pohl ol pcilrttttl 

l7utvadr+ F.rhral dilGll 

lubilcrlle 

htdrsl.|| 

Affico6oyo.d 

ffirbr.r 

ilrr|cli 

lortrnt 

l-*T { *'s. t 

Vrshr 

, h€hlopuslc rrdra 

Eclbdcrfiliott|| 

nt ttL 

ht.rb. trtcla ol 

rroCtn||al CaF{tltgn 

Pdlnl 

rf pal|l||rl 

ErlTtrrl rDHdctrt 

ol rnrl ctial 

Fig. (5): The levator ani muscles 

ArccocE gill lgtrfrtnl 

+ 

$ymphyttc publt 

Fuboraalrflr muroh 

# 

Fig (6): Puborectalis muscle. 

Anorectal ring 

Aggregation of circular muscles firstly described by 

(MilliGan and MorrGan, Ig34) lies at the anorectal Junction composed of 

* 

aggregation of LA.s., E.A.s. and puborectalis sling forming strong ring 

weak anteriorly.

Anal Flrula 

Review af Llterature 

It can be felt digitally as an abruptly terrrinated posterior edge above 

which the cavity of rectum is felt. 

+ Anococcygeal Raphi 

fr 

Layered musclotendinoustructure in mid line between'anorecfum 

and coccyx 

from above downward its layers are 

. Presacral fascia 

. Tendinous plate ofpubococcygus. 

. Muscularaphe of puborectalis and E.A.S 

(Wendell-smith& Wikon 1977) 

Para-anal and Para-rectal Spaces: There are several important 

potential spaces in the anor€ctal region that have surgical relevance. 

t 

The apex of the ischiorectal space is at the origin of the lsvator ani 

mu$cles frorn the obturator fascia 

Fig.(7,9). This space is bounded 

inferiorly by the perineal skin, anteriorly by the transverse muscles of the 

perineum posteriorly by sacrotuberous ligament and gluteus maximus 

muscle, medially by the EAS and levator ani, and laterally by the external 

obturator muscle 

t 

In the lateral wall of this space is Alcock's canal through which the 

pudendal vessels and nerves course. There is a potential extension of this 

space anteriorly, which courses above tlre urogenital diapluagm. 

The contents of this space include fat, the inferior hemorrhoidal 

vessels and newes, and the scrotal or labial vEssels. 

rl

Anal Flsmla 

Revlsr|v of Literatare 

The perianal $pfrce (Fig.7, 9) sunounds the anal verge is 

continuous with the fat of the buftocks laterally, and erctends into the 

intersphincterie space. Its contents are the most saudal part of the EAS, the 

external hemonhoidal plexus, and the inferior hemonhoidel vessels. This 

space is bound down tightly because the comrgator cutis runs tluough it. 

The interSphincteric spAce (see fig 7) is a potential space between the 

IAS and the EAS is continuous with the perianal space. 

The bilateral supraleyator space$ (fig. 7, I and fig. 9) are 

bounded superiorly by the peritoneum, Iaterally by the obturator fascia, 

medially by the rechm, and inferiorly by the levator plate. These spaces 

can connect to each other posteriorly behind the rectum, deep to the 

anococcygeasl raphe but superfioial to the rectosacral fascia. 

The submucoutt space begins at the dentate line and Extends 

cranially to join the gubmucosa of the rectum proper. The internal 

hemorrhoidal plexus is in this space. 

The superficial po$tflnal $pflce (Fig. 8) is continuous with the 

superficial ischiorectal fossa posteriorly, deep to the skin but superficial to 

the anococcygeal li gantent. 

+ 

# 

# 

The deep po$tanfll $pf,ce (Fig 8), in conrast, corulects the deeper 

parts of the ischiorectal fossa together posteriorly behind the anal canal, 

deep to the anal coccygeal ligament but superficial to anococcygeal raphe. 

Horseshoe abscesses usually occur through this space but also may occur in 

the superficial postanal $pase (Fig.g). 

The rrtrorectal 

spflcc (Fig 8) begins cranial to the retro $acral 

ligament betweEn the the rectum and the $acnrrn and is continuous with the 

t 

l2

Anal Fbtula 

Review ofLiterature 

t 

refio peritoneal space above. Its boundaries are the fascia propria of the 

rectum'anteriorly, the presacral fascia posteriorly, and the lateral rectal 

ligaments laterally. This plane is avascular , the fascia propria protects the 

mesorectal vessels, and the presacral fascia invests the presacral vessels. 

Lovalof E.rl rI| rcl. 

f 

Erlrrtr$l anef sphlncter 

lfllrrDtl 

rphft'rclet 

Fig. (7): Coronal diagram ofthe para-anal and para rectal spaces. 

t 

rptcc 

R*to|.Eillfracb 

S||tf,rbu.atd 

+rrE. 

;Lrvrld 

||{ 

DtaP pothrrf rotc, 

I Affl c$oygEut ;ermfirl 

- i 

8u9.tfl6hl For|rhcl 1415cr 

t _ 

f 

Fig. (8): Lateral diagram of the posterior spaces

Anal Fbtula 

Review of Lileralure 

gup.tlty.tor 

I 

i 

Intrrrphthot.rf 

||chlorc€t11 rl 

Pcrltnrf rplcr 

Fig (9): Coronal diagram of the para-rectal and para-anal spaces 

illustrating how an abscess can track posteriorly from one lateral space to 

gain access to contralateral space. 

t 

Blood Supnlv 

The major arterial blood supply,to rectum and anal canal is provided 

by superior and inferior hemonhoidal arteries whereas the middle rectal 

artery has variable contribution depending on the size of superior rectal 

artery 

Venous drainage 

l 

Venous drainage of rectum and anal canal runs with arterial supply, 

f)rainage tluough superior hemonhoidal vein is into the portal system, 

Drainage through middle, inferior hemorrhoidal veins is into internal 

iliac veins to inferior vena cave i.e. svstemrc 

I 

There are free anastomosis between all of these venous channels.

Anal Fhtula 

Reviev, of Literatwe 

LYmphatic drainage 

'Recfitttt 

t 

Upper 213 of rectum ascends with superior rectal vessels to reach 

inferior mesenteric nodes. 

Lowerl/3 drains not only into inferior mesenteric nodes but also into 

intemal iliac nodes. 

* 

Anal canal 

Above dentate line like lower l/3 of rectum 

Below dentate line to inguinal lymph nodes but can be to inferior 

mesefiteric nodes and nodes along inferior hemorrhoidal anery. 

+ 

Nerve supply 

I,A.S. 

r Motor supply is sympathetic L5 and parasympathetic 52, 53 

and 54. 

r Tone is mediated by both sympathetic and parasympathetic. 

r Contraction is predominantly sympathetically mediated. 

r Relaxation of I.A.S. is part of intramural reflex. 

r Distention of rectal wall above anorectal ring leads to relaxation 

of I.A.S. 

+ 

c'.1..f. 

r Motor supply is pudendal newe (S2, 53) and perineal branch of 

s4. 

l5

Anal Fbtula 

Rwtwof Literutnn 

Lantor Anl 

Puborectalis 

. Pudendal nerve alone 

r Direct pelvic branches of s3 s4. 

. Combination of both 

* 

Iliococcyqeus and oubococcveeus 

r Superior aspects by s4 

r Inferior aspects by perineal branches ofpudendal nsrves 

' 

Sentorv 

r fuial canal from skin below up to l-1.5 cm above dentate line 

epithelum contains 

. Messneros eorpuseles (Touch) Krause's bulbs (cold) Golgi- 

Mazzoni bodies (pressure) and genital corpuscles (Friction), 

r Sensation earried through inferior hemonhiodal branch of 

pudendal nrirvE. 

r Rectum above that level is only sensitive to distension through 

receptors out side rectal wall it self to parasyrnpathEtic nerves 

s2, s3 and s4. 

t 

* 

# 

l6

Anal Flstula 

R*iew of Literature 

DEMOGRAPHIC STUDY 

* 

There is no age exempt regarding anal fistula but it is more frequently 

nr*t rvithin the middle years of life (lllitson, 1964), 

'l'lrey.are uncommon after age of 60 years (Vasilntsky and Gordon, 

.-,ooo,, 

There is male dominance in every reported series, male to female raiio 

in 5 years review at St Marks Hospital was 4.6:l (Marks and Ritchie 

1977). Similaratio was reported by Shouler et aI, (1986). 

if 

In Nigeria the male dominance is 8:l (lnf and Solanke, 1976). 

This male dominance is explained by Golligher by the less fastidious 

attitLrde of men in general towards anal cleanliness, rougher type of 

underclothing and more work causing more sweating 

anal region. 

il 

+ 

l7

AnalFbtula 

Revi*t olkteratare 

AETIOLOGY 

Either congenital fistulae whose formation are not related to abscess 

formation at any stage and these fistulae are usually lined by epithelium or 

acquired fistulae showing the abscess-fistula sequencE in their pathogenesis 

in conffasthese fistulae axe lined by granulation tissue. 

] 

The second group can be divided into subtypes according to the 

mechanism of abscess formation either traurnatic, infective or other causes. 

I- Consenital 

Congenital Perianal fistulae have been reported in early infancy 

(Duhamel, 1975; Fitzgerald et aL, I98S). And in some cases the tracks 

are lined by columnar or fiansitional epithelium suggesting that these might 

have a developmental origin (Pople and Ralphs, IISS), 

f 

II- Acquired 

Acquired anorectal abscesses and fistulae have a conrmon cause, 

indeEd, the term fistulas abscess has been used to describe this problan, the 

abscess is an acute situation, whereas the fistula is a chronic orte. 

* 

Most fistulaq occur after drainags of a previous anorectal abscess, but 

not all abscess are oomplicated by a fistula and not all patients with fistulae 

give a history of previous sepsis (Marhs and Ritchie, 1977). 

t 

Numerous conditions may play an etiologic role in formation of a 

fistulous abscess. 

l8

Anal Fbtula 


According to the mechanism of abscess formation acquired fistulae 

may be infective, tralrmatic and others. 

: fl' A- Infective ftstulae 

On top of a pathologically demonstrable disease or otherwise 

apparently healthy organ. 

L lnfective fistulae due to bowel oreanism with no demonstrable colorectal 

disease. 

*. 

' 

They form the majority of perianal fistulae. 

Infection of anal glands is probably the most corlmon cause of 

fistulous abscess (Eisenhammer, 1956; Park's, 1976). 

t 

Parks and Morson demonstrated infected anal glands in 70% of cases 

and histologic evidence suggestive of this orign in another 20% bringing 

the total to 90% (Park's, I96I). 

Goligher found inter sphincteric abscesses in only 23% of anorectal 

abscesses suggesting that this cause is less often the precursor (Goligher, 

1967). 

+- 

However, this theory is supported by the fact that internal opening is 

found at level of pectinate line in most cases. 

l9

Anal Fistula 

Revle* of Literature 

This hy?othesis postulates that infection starts in anal gland lying 

within inter sphincteric plene at line of anal valves (dentate line). 

As the abscess expimds pus may traok longitudinally, up or down, in 

the inter sphincteric, submucous or extra sphincteric planes to present as a 

perianal, ischiorectal or supra levator abscesses. 

f 

Circumferential tracking can similarly occur along these planes to 

form horse shoe abscess. The fistula is complete when the abscess 

spontaneously discharges or the surgeon prOvides this corununisation. 

Secondry fiacks complicate the situation rspresent upward extension 

into the supralevator $pase or lateral extension into the ischiorectal fossa 

(Lnttimer et aL, 1996). 

* 

2- lnfectiVe fistulae on top of a patholoeicallv demonstrable disease. 

Binderow and Wmner, (1994) stated that abscess-fistula secondary to 

specific infection conrprornise less than l09o of total nurnber of abscess. 

* 

l- On toa af demonstrable specific in{ection of orwrl. 

A. Tuberculosis: 

- Route of infection of anal region 

* 

L Open pulmonary cases through swallowed sputum. 

spr.ltum on hand during anal toilet or blood bom- 

Rarely by 

20

Anal Fkula 

Revlew ofLiterature 

+ 

* 

2. Healed pulmonary lesions Here inoculation of perianal region wittr 

tubercle bacilli took place considerable time previously. They 

remained dormant in tissues till a decrease in local or general 

resistance occur or till soms superadded pyogenic infection leading 

to the production of an abscess and a fishrla occllrs. 

3. Lymph nodal disease tluough blood spread (Goligher, 1984) 

4. infection of anal region by bovine type ingested in infected milk. 

5. Very rarely direct extension. from tuberculous lEsion of the hip, 

sacrum, prostate or seminal vesicles (Goligher, 1984). Tuberculous 

anal fistulae are much less cotnmon today than at the turn of the 

century (Melchior, I9I0), Or a-round world war II (Buie et aI,1939, 

Jackman and Buie, 1946). 

Even in Africa, tuberculous fistulae are becoming less common 

(Eisenhammer, 1978). Ani and Sakmke, 1976 reported only 4 cases (5%) 

in their series of 82 patients in Nigeria with intestinal tuberculosis. 

^ 

* 

Tuberculous anal fistulae are still evident in over 15% of anorectal 

fistulae found amongst lndian citizens in their own country $hukla et aL, 

1988). 

No specific clinical features and diagnosis can only established by 

histopathological examination detecting epitheloid giant cells wluch is 

,+ rnuch nrore reliable than the presence of acid fast bacilli. However we can 

suspect lesion to be tuberculous depending on patient criteria and local 

criteria. 

2l

Anal Fbtuh 

Rwtuwofhturatuft 

Reqardine patient 

AIDS patients, those on steriods or patients from endemic areas (Bode 

et ilL., 1982). 

f, 

Resardins local clinical criteria 

Detection of abscess in presence of a suspicious ulcer, indruation or 

anal stenosis may be suggestive (Keighley, 1993). 

If external opening on the skin is ragged, induration is mild or absent 

and if the discharge is watery (Farthing et aI,I993). 

Unsuspected tuberculous anorectal lesion may b€ the cause of 

recurrent anorEctal sepsis and recunent fisfulae after adequate surgery 

(chrabot et aL, 1983). 

fl, 

Resolution of tuberculous anorectal manifestations can be expected 

foll owin g chernothera py ( F art h ing et n L, I I I 3 ) . 

B- Actinomycosis 

caused by actinomyces israelli anaErobic branching gram positive 

organism normally found in mouth. 

l 

Actinomycosis of rectum is very rare it may be prinary or secondary 

following spread from proximal bowel involvement. 

# 

Presented by indurated perineum with multiple fistulae discharging 

the typical actinomycotic pus containing sulphur granules. 

22

AnalFhtula . 


These lesions will heal completely with appropriate microbial therapy 

particularly tefr acycline. 

t 

C- Sexually transmitted diseases complicated by anal fistulae: 

l- Lvmoho sranulomavenenrm caused by chlamydia trachomatis virus 

sero types Ll,L2 and L3. 

Clinically prominent inguinalymphadenopathy foltrowed by anorectal 

strictures. Recurrent anal and ischio rectal abscess are common in this 

condition with resulting fistulae fonnation . 

* 

Diagnosis by tissue culture of rectal biopsies or complement fixation 

test (Gittitand antl ll/'exner, 199n. 

7." AIpfi 

t 

Caused by HIV which suppresses immunity and allows the 

development of malignancies and oppornrnistic infections (CMV,HSV, 

pneumocystis carinii pneumonia). 

t 

Perianal disease in the form of arral warts, sepsis is common in male 

horno sexual irrespective to their HIV status (Miles and lVastell, 1991). 

Usually perianal suppuration presents late in these patients as they are 

commonly on long term antibiotics for varied reasons.

Anal Fbuh . 

Revicv of Literelure 

" 

Intersphincteric abscess with or without fistulotrs connectiort' ohronic 

and complex abscesseg are seen to bE more common in ccnter of disease 

control group III &IV. 

Severe progressive sepsis has been reported in AIDS patients but 

doesn't seem to be common finding (Sim, 1988). 

# 

n- f a m;jt jgjtfe c t i on s. 

l- Amoebiasis: 

Caused by entamoeba histolitica. The lesion are maximally met 

whinin the caecum and the rectwn which comprise the main primary sites 

(Etwi and Anwer, 1967). Spreading of amoebic infection to perianal 

region after operation or traumatic injwies can occur in patient with 

chronic intestinal amaebiasis (Nevin,I 947). 

.fr 

Nen+ich and Maskatt (1946) had noted an amoebic ulcer of buttock 

connected to a para rectal abscess 

2- Bilharziasis 

is ccnsidered uncomrnon underlying factor in pathogenesis of fistulain-ano. 

f 

Peri anal fistulae occur either by suppuration of subcutaneous deposits 

of bilhanial ova which oscur mainly in perineurn, ischiorectal fossae and 

buttocks and this tacks inwards into urethra or recturn resulting in urinary 

or anal fistulae or less comrnonly by septic infection of bilharzial ulcer of 

rectum which tracks tluough the perirectal tissue to the skin. 

rt. 

24

Anaf Fbtula 

Review ofLiteralure 

In study Oon* io Egypt in 1970 on 206 cases of anal fistula 49 patients 

of them proved to have bilharziasis only 5 ,rr*, oi anal fistulae proved to 

+ 

be caused by bilharziasis i.e. less than 3% of total cases of anal fistulae. 

E- Cytomegalovirus 

Cytomegalovirus (CMV) is a common human viral infection, affecting 

40 % to 100% of adults. Acute infections are frequently asymptomatic , but 

the infection is acquired, there is lifelong latency coupled with the'risk for 

interminent reactivation. Although gastrointestinal CMV disease can oscur 

in persons with normal immune fi.rnction, it most frequently occurs in 

adults with immune deficiency, suclr as the acquired immunodeficiency 

{* 

syndrome (AIDS), organ transplantation, cancer chemotherapy, and steroid 

therapy. Because the number of patients with immune deficiency has 

increasedramatically in recent years, and because CMV is one of the most 

conunon infectious complications in these settings, the number of patients 

with CMV disease is also increasing. New diagnostic tests and treatments 

have been developed to help physicians address this growing problem. 

# 

t 

Cytornegalovirus can damage many organs, including the lung, retina, 

liver, and gastrointestinal tract. This review describes the pathogenesis of 

gastrointestinal CMV disease, the types and locations of gastrointestinal 

lesions, the clinical settings in which they occur, and the specific methods 

available to diagnose and treat the disease. 

25

AnalFkruh 

Revlprt olLiterutwrc 

Pathosenesis 

Primant Infeetion and Latencv 

Most CMV infections are acquired either in the pErinatal period and 

infancy or in adulthood through sexual contacts (HO, 1990. ) 

# 

Although congenital infections due to primary CMV infection in 

pregnaricy af,e a cause of substantial morbidity and death (Demmler, I99I), 

Most primary CMV infections in immunologically healthy adults are 

asymptomatic or are associf,ted with a mild mononucleosis like syndrome. 

Serious gastrointestinal disease due to primary infection is rare (see below 

in "Healthy persons"). All primary infections resolve and enter a state of 

latency in which live virus is sequestered in a non replicative state. Persons 

with latent infection have no symptoms but do have antibody to CMV. 

s 

The predominantissue site of viral latency is not known (Rabin 

1990) but circulating lymphocytes, monocytes, and polymorphnuclear 

leukocytes all probably contrilin latent vinrs (Merigan 1990). 

# 

Organs. at risk for subsequent CMV disease, including the 

gashointestinal ttact, may contain latent virus that may cause local disease 

with reactivation (Tyms et atr., 1989) 

Inf'ect ion C ompared with Disease 

t 

Because most patients previously exposed to CMV have latent vinrs in 

various organs without evidence of organ damage, infection with CMV is 

26

Anal Fhtula 

Revlew ofLilerature 

* 

more coilrmon than disease caused by CMV. In pregnant women, 

intermittent asymptomatic viraemia and vinria, hot associated with organ 

damage, are common. In immunodeficient patients, CMV infection can be 

detected (see below," Diagnostic Techniques") in salivary glands and 

saliva as well as in the kidney and urine; however, substantial CMV disease 

in these organs does not occur (Grundy lgg0) 

Asymptomatic infection of the gastrointestinal tract has also been 

detected (see below). Therefore, the identification of CMV in tissue or 

body fluids may indicate infection but not necessarily disease. 

+ 

Some authors have suggested that gastrointestinal CMV is frequently a 

nonpathogenic bystander or secondary invader (Gangahar et aI 1988) 

+_ 

t 

Furtherrnore, it has been suggested that the presence of CMV in areas 

of inflammation reflects the propensity of the virus to infect rapidly 

growing tissueso especially endothelial cells in granulation tissue 

(Goodman et al., IgTg) Clearly in an individual patient, the clinical 

significance of finding evidence of tissue CMV infection may be unclear. 

For example, an AIDS patient with endoscopic evidence of esophageal 

Candida infection may have detectable cytomegalicells (Figure l0) in a 

mucosal biopsy or cytomegalic cells may be seen in an area of gastric 

inflammation that also contains Helicobacter Pylori; or, a colonic biopsy 

taken from a patient with an exacerbation of chronic ulcerative colitis may 

show the presence of CMV( Berh et aI, 1985). However, strong evidence 

exists that CMV is a true gastrointestinal pathogen: I)CMV is often 

detected in the absence of other pathogens;2 )the severity of the mucosal 

lesion reflects the number of CMV- infected cells (Hinnant et aLI986) 

21

Anal Flstula , 

Review of Literuture 

antiviral therapy benefits patients wrttr histotogically sonfirmed disease; 

and 4) in patients with persistent immune deficiency( for example, AIDS), 

virologic, histologic, and symptomatic relapse occurs after cessation of 

antiviral therapy. 

f 

A reasonable definition of cMV intestinal disease(as opposed to 

infection only) is an erosive or ulcerative process in the wall of the gut in 

which the presence of cMv is shown by routine histologic examination, 

culture, or antigen or DNA staining, in a person in whom other 

explanations for the lesion (s) have been excluded. 

# 

Fig. l0: Endoscopic gastric mucosal biopsy specimen from an AIDS 

patient with severe nausea, vomiting, and epigasric pain.showing tlpical 

cytomegalic cell shows a large, densely stained nucleus with 

intracytoplasmic inclusions (original maginfication x400). 

# 

f, 

React ivat ion and Re infection 

cytornegalovirus disease in the setting of immunodeficiency can be 

the result of either a primary cMv infection in a previously uninfected 

?8

Anal Fbtula 

Review o! Literature 

(serbnegative) host, reactivation of latent virus, or reinfection with a new 

virus (Grrndy 1990.) Most CMV disease is due to reactivation of latent 

t 

virus (IIo 1990.) reactivation is associated with adequate anti-CMV 

antibody but defective cell-mediated immunify, characterized by decreased 

numbers of cytotoxic T lymphocytes and nahrral killer cells (Ruhin lgg0.) 

In theory, the frequent occurrence of esophagogastric and colonic CMV 

disease in patients with AIDS could occur because homosexual men 

swallow CMVJaden semen or engage in reeeptive anal intercourse. 

However, cMV of the esophagus and colon are common in transplant 

'# 

patients who are not at such high risk for direct gastrointestinal CMV 

inoculation. Furthermore, the frequent occurrence of CMV retinitis in 

AIDS patients is unlikely to be due to direct inoculation of new virus 

snbffies. In both AIDS and organ transplant patients, the incidence and 

severity of gastrointestinal CMV disease closely parallel the degree of 

cellular immure dysfimction, suggesting that CMV disease is related more 

closely to the severity of immunodeficiency than to the source or subtype 

of virus. - 

l 

+ 

Gast rointes t inal C vto mesal ov i rus D isease 

The organ system manifesting cMV disease varies depending on the 

cause of the host's immunodeficiency. For example, pneumonitis is more 

common in bone rnarrow transplant patients, but retinitis and 

* 

gastrointestinal disease are more common in ArDS patients (Ho, Igg0). the 

factors that rnake the intestine vulnerable to cMV injury are unknown. 

In gastrointestinal CMv disease, the gross appearance and location of 

the lesions are similar regardless of the cause of the host's 

29

Anal Fk*uh . 

Revlew otLiterature 

immunodeficiency (Griffiths, l98E). Ulcerations, erosions, and mucosal 

hemonhage are the primary macroscopic findings. Although such lesions 

may have other causes, microscopic identification of the eytomogalicell 

provides evidence of tissue infection vyith CMV (see below, 

"Histopathology') (Hinnant et aL 1986) Special stains for CMV antigens 

aird DNA have shown that many more cells are infected than those that 

have classic cytomegalic changes (Hinnnnt et aL 1986.\ many 

gastrointestinal cell types can be infected in active disease, most commonly 

vascular endothelial cells but fibroblasts, smooth muscle cells, and 

glandular epithelium are also infected {Hinnant et aL 1986.) Figure ll. 

f 

The pathogenesis of intestinal lesions recently been reviewed( 

Grrmdy. Igg0). it is a complex process involving mucosal CMV infection 

with inflammation and tissue necrosis and vascular endothelial 

involveurent with subsequent ischernic mucosal injury (Iwasaki 1987.) 

vascular occlusion may be an important cause of tissue injury . however , 

surface epithelia! cells columnar, never squamous are frequently infected 

at the edge of the uleerations and in nearby mucosa that is not inflamed 

(Foucar, ef aL l9&I).results suggesting that vascular involvernent is not 

necessarily the only or predominant cause of tissue injury. Local immune 

suppression or autoimm$ne factors may play role in the pathogenesis of 

gastrointestinal CMV disease (Merigutt, et al. 199A.) btrt they do not 

appear to be central to the pathogenesis as they are in CMV pneumonitis in 

bone marrow transplant recipients( Grundy. 1990.) 

U 

# 

I 

30

Anal Flstula 


l 

u 

Fig. I l: Routine histiologic section frorn an AIDS patient who had a small 

bowel resection for perforated ulcer. Left, the many cytomegalicells show 

infection of various cell types including vascular endothelium (small 

arrow), fibroblasts (rnedium anow), and smooth muscle cells (large anow) 

(original magnification x 200). Right, most of endothelial cells in the three 

blood vessels shown are cytomegalic. Ischemia as a result of vascular 

occlusion may be irnportant in the pathogenesis of ulceration (origrnal 

magnification x 200). 

Gastrointestinal Cvtomeqaloviru.t Disease in Different Hosts 

'lt 

Gastrointestinal cMV disease is suspected when gastrointestinal 

symptoms or lesions develop in a patient with a recognized high risk for 

CMV disease. 

The Acuu i re d I m mztn r ilefic i enc v Svn dro me 

+ 

As discussed above, rnost AIDS patients have serologic evidence of 

cMV infection (Jacobsort et al. 1988.) and the virus can frequently be 

isolated frorn body fluids (Quinnan. et aL 1g84.) lmportant inleraciions 

between human imrnunodeficiency vinrs (HIV) and CMV have been 

reviewed (Schooley. 1990) In AIDS patients, the risk for CMV disease 

increases when CD4 counts decrease to less than 100/mmt (Dre*.198f ) 

3l

Anal Fbudr . 

Raview of Llterature 

Cytomegalovinrs diseasE is the most common serious opportunistic 

Pathogen. Gastrointestinal CMV disease is the most common cause for 

emsrgency or elEctive abdominal $urgery h AIDS patients( Franh 1984), 

Patients with AIDS can have CMV disease of any site in the 

gastrointestinal ffact, including the mouth( Marcusen et aI 198f.) 

esophagus (Wilcox et aL 1990). Stomach (Hinnant et aL 1986.) small 

bowel( Fernandez. et aL I9E6). appendix ftln et aL 1990.). and colon 

(Frank et el 1984). Primary peritonitis has been reportedf lfiilcox et aL 

1990.) 

t 

Orsqn Transnlant Recini4t1 

Cytomegalovirus is the most conmon infectious complication of 

organ transplantationn occurring in 60% to 70% of kidney, liver, bone 

marrow, and heart transplant recipients( Rubin 1990). At lest one half of 

these infections are symptomatic. Gastrointestinal CMV disease occurs in 

about l0% of all transplants( I|'Ieyers et aL 1990). Three descriptive 

studies have documented a high incidence (30% to 507o) of asymptomatic 

CMV infections in endoscopically normal gastrodudenal mucosa during the 

frrst month after transplantation( Spencer. et aL 1986.) However , as in 

AIDS patients, symptonratic gastrointestinal CMV has been otserved in all 

parts of the gastrointestinal fract, including the esophagus( Spencer. et aL 

IgSd), stomach, small intestine( Spencer. et sL 1986),and colon 

(Gangahar. et al. I 988.) 

# 

Case reports and postmortem series have documented severe 

ga$trointsstinal CMV disease in'this group of patients mostly in those with 

myelo- or lymphoproliferative disorders, particularly thoss treated with 

steroids (Naheshim* et aI 1992.1 Oastrointestinal CMV disease was 

described in rancer patients well before the AIDS and uansplantation eras 

(Goodman et aL l9lSJ,Although CMV ulcers sometimes have preceded 

the diagnosis of cance( Furukawa. et aL 1988), more commonly they 

have complicated thE clinical course of a patient with an established canser 

Nabeshima. et al. 1992.) 

Steroid Therapv 

Oral, gastric, duodenal, and colonic lesions that contain cytomegatic 

cells have been reported in association rvith steroid therapy (Orlolfi Et al. 

1989). in patients with cancer (see above); with rheumatic disease (Kanas. 

et nl. 1987.) and with asthma (Nabeshima et aL 1992.) Several pathologists 

have suggested that steroid- associated peptic ulcer disease is, in fact, 

* 

I 

32

Anal Fbtula 


+ 

* 

C.M.V disease of the stomach and duodenum (,Rosen et aL lgTI). 

Evidence derived from case series provides support for this concept in 

some patients (Hanson I 972). 

I nfl ammatortt B ow e I D is ea s e 

The relationship between inflammatory bowel disease and CMV has 

been reviewed (Berh et aLI985). Evidence from case reports published 

dwing the last 20 years shows that l) CMV colitis can mimic the clinical 

features of acute idiopathic proctocolitis (Cunningham et aL 1986.) 

2) acute CMV colitis can . initiate a clronic disdeasa indistinguishable 

clinically, endoscopically from ulcerativd colitis (Diepersloot et aL1990.) 

in patients with exacerbations of ulcerative colitis and toxic megacolon, 

cytomegalicells may be detected in colonic biopsy or surgical specimens( 

Eyr*Brook et aL 1986.; and 4) patients with exacerbations of ulcerative 

colitis, which are resistant to steroid therapy, rvho have cytomegalicells in 

mucosal biopsy specimens, rnay improve clinically and histologically after 

steroid withdrawal (Berlt et aL 19851. In such patients with ulcerative 

colitis and cytomegalicells in rnucosal biopsy specimens, it is unclear 

whether the CMV is localizing in areas of pre- existing inflammation or 

whether the virus is causing disease( Eyre-Brook et al. 1986). 

other Immunodeliciencv States: the late- onset adult immunodeficiency 

syndrome has been associated with gastrointestinal CMV disease 

(Freeman. et al. 197n. including gastric erosions and severe ch'ronic 

colitis. 

Elderlv Patient:s 

* 

A small number of patients older than 65 years, without other illiress, 

have had gastrointestinal CMV disease including colitis( Spiegel et al. 

1980.) gastric ulcer (Levine. Et al. 1964). and small bowel perforation 

(Henson. 1972). Follow -up observation and detailed immunologic studies 

in these patents are lacking 

Healthv Persons 

s 

A descriptive study published in 1964 suggested that CMV may cau$e 

gastrointestinal disease in patients without detectable immunodeficiency 

(Levine et al. 1964). Immunocornpetent patients have developed 

gastrointestinal CMV disease associated with community- acquired, acute 

primary CMV infection (Cunninghum et al, 19S6). blood transfusions 

(Campbell. Et aL 1977). or sexual transrnission (Rabinowitt Et aL 1988). 

Several authors have reported( Lachmut. et al. I97I), an acute, self limited 

gastropathy in children, associated with marked hypertrophy of gastric 

33

Anal Fbtuh R*lat of Llterature 

folds and protein- losing enteropathy- These patients had serologic, 

histologic, or cultrrre evidenoe of CMV infection, or all three. 

I- Clinical Presentation and sites of lnvolvement. 

Table L Clinical Featwes Suggesting Possible Gasuointestinel 

Cytomegalovirus Disease 

a) Hi 

d immunodeficiency syndrome 

: reclptent 

I theiaov 

or Can'c'er chemotherapy 

3 

Abdomlnal Darn 

Colities or bloodv diarrhea or both 

Acute abdorien 

c) ' Gastrointestinal lesions 

Esonhaqeal ulcer 

GastriiulcEr 

Gastric ulcer 

a- Mouth 

Painful etosions or ulcers (Marcusen and sooy,1985 ), enlarged, 

painful salivary glands (Pialoux et al, l99l), and odynophagia due to an 

epiglottic (Hinnant et al, 1986 ) or posterior pharyngeal ulcer (Laiwani et 

al, l99l). 

b- Esophagus 

A large, solitary, distal esophageal ulcer caused odynophagia or 

constant substerlral pain or both in AIDS patients (McDonald et al, 1985). 

Esopagnal strichue formation after healing with anti-CMV therapy has 

been described (Wilcox et al, 1990 ), 

c- Stomrch 

Epignsfiic pain, nanrsea, and vomiting (see Table l) (Iwasaki, 1987), 

Complications of CMV gasnic ulcers inolude bleeding (Allen et al, 

lgSllgastric outlet obstrucfion (Victoria et al, 1985), and perforation. 

d- Small Intestine 

Asymptomatic trarrsplant recipient wi th endoscopically normal 

duodenal mucosa (Franzin et al, l98l ) to a patient with progressive 

diarrhea followed by fatal perforation of a severely ulcerated mucosa 

(Fernandez et al, 1986). Terminal ileal disease may mimic Crohn disease 

clinically, and radiologically (Wajsman et al, 1989). Small-bowel erosions 

and ulcerations have been observed in a healthy adult with acute CMV 

infection (Spiller et al, 1988) and in an elderly patient with no apparent 

immune disorder (Spiegel and Schwabe, 1980). Cytomegalovirus 

ulceration of the appendix has occuned as acute appendicitis in AIDS 

patients (Lin et al, 1990) 

* 

3 

fr 

34

AnalFbtula 


* 

e Colon: 

Diarrhea, hematochezia, urgency, tenesmus, and abdominal pain, 

often with associated constitutional symptomsuch as fever, malaise, 

anorexia, and weight loss (Frank and Raicht, 1984). The presentation can 

be acute (Tamura, 1973) or chronic (Frager et al, 1986). Massive acute 

bleeding has been reported (Goodman and porter, 1973), especially from 

cecal ulcers in transplant patients (Foucar et al, l98l) Colonic perforation 

has been described frequently (Gangahar et al, 1988). 

II- Diagnosis 

Table 2 Methods Used To Diagnose Gastrointestinal Ctomegalovirus 

Disease 

Acceptable and specificity 

svol( 

Uncertain sensi 

and specificitv 

rre of lesionschain 

reaction on tissue from lesion 

i* 

+ 

* 

The best approaeh is to confirm the presence of CMV with histolo 

analysis and to nrle out other pathogens using standard techniques. 

a- Serologic Analysis 

Because of the high prevalence of IgC anti-CMV antibodies in most adults, 

this assay is not helpful as a diagnostic tool to detect CMV disease 

(Culpeper-Morgan et al, 1987) the presence of IgM_anti-CMV antibody - 

suggests recent infection but does nst establish the diagnosis of tissueinvasive 

disease (Merigan and Resta, 1990), 

b- Blood, Urine, Stool, and Oropharyngeal Culture 

A positive test result frorn blood, throat, or urine culhrre does not 

prove that gastrointestinal signs or symptoms are due to CMV disease nor 

does a negative culture from these sites rule out gastrointestinal CMV 

disease (Culpeper-Morgan et al, 1987). Quantitative polymerase chain 

reaction (PCR) assays on blood may be more useful than culture in 

predicting active CMV disease. 

c- Radiology 

Barium radiographs from patients with proved CMV disease have 

been published (Bafthazar et al, 1985). In the esophagus, the most corrmon 

finding is the distal, solitary ulcer, In stomach, thick gastric folds, antral 

narrowing, or ulcers, have all been described (Balthazar et al, 1985). Ileal 

narrowing r:esernbling Crohn disease has been observed (Wajsman et al, 

1989). ln the colon, the raiographic findings can be focal or diffuse, and the 

mucosal changes may be superficial or may be deep ulcerations (Balthazar 

et al, 1985). These radiographic findings described above are nonspecific. 

35

.a"nal Fbtula 

Review of Lllerature 

d- Endoscopic exflmination 

The definitive diagnosis of CMV gastrointestinal disease depends on 

invasive procedues and biopsies. Upper (Wilcox et al, 1990) and lower 

(Rene et al, 1988) gastrointestinal endoscopic examinations of CMV 

disease usually appears as a mucosal erosion or ulceration. Full 

colonoscopic examination may identify more patients with CMV colitis 

than does flexible sigmoido scopic examination (Dieterich and Rahmin, 

ree.l). 

*- Histopathologic Analysis 

.t characteristicytopathic effect: a large 25 to 35 pm cell 

cantaining a basophilic inffanuclEar inclusion, which is sometimes 

surrounded by a clear halo ("owl's eye" effect) and is frequently associated 

Muly with clusters of intracytoplasmic inclusions (see Figure l0) 

studies have confirmed the specificity of cytomegalic cells for diagnosing 

f"JIvlV.antigen because they are always associated with CMV antigan or 

CMV DNA (Eyre- Brook et al, 1986), or both, as shown by special staining 

techniques. However, in some proved cases of gastronitestinal CMV 

disease, cytomegalicells may be rare and difficult to detect (Myerson et 

al, 1984), requiring great time and effort by the pathologist (Culpepper- 

Ir4organ et al, 1987). Success in finding these cells is a function of the 

number of biopsy specimens examined and the diligence of the pathologist 

(Goodgamet al, 1993). This lack of sensitivity is a disadvantage of 

routine histopathologic examination. 

e- Culture of Mucosal Biopsy $pecimens 

Culture of endoscopic biopsy speciments adds expense that may not 

be justified by an improvement in diagnostic yield when compared with 

routine histopathologic analysis coupled with a vigorousearch for 

cytomegalicells. 

f- Immunochemicfll Staining of Histologic Specimens 

lmmunoperoxidase or immunofluorescence staining for CMV 

antigens using rnonoclonal antibodies (Culpepper-Morgan et al, 1987) and 

in-situ DNA hybridization using a biotinJabeled probe, whereas antigen 

staining indicates viral replication, DNA staining ocflrs with latent viral 

infection. Two studies (Francis et al, 1989) reported that the 

inrrnunoperoxidase stain was positive when routine histologic analysis 

failed to show cytomegalicells. In a study of 80 symptomatic AIDS 

patients who had gastrointestinal mucosal biopsies, l3 of 80 biopsies 

(16.3%) were positive for CMV using in-situ DNA hybridizationl. Tested 

in these same l3 biopsy specimens, the immunoperoxidase stain (7 of 13 

positive) and Histopathologic stains (5 of l3) positive were less sensitive, 

g- Polymerase Chain Reaction 

In this small pilot study in AIDS patients, PCR had greater 

sensitivity for detectin gastrointestinal CMV disease than culture and 

immunoperoxidase stain. However, PCR is a technique with many 

technical pitfalls and is not standardized for CMV diagnosis. 

r 

* 

# 

r 

36

Anal Ftstula 


+ 

t 

t 

t 

III- Treatment 

Only supportive therapy is needed (Campbell et al, 1977). However, 

with rare exceptions (Levinson and Bennetts, 1985), the evidense strongly 

suggests that in the absence of the therapy, gastrointestinal CMV disease in 

a host with sustained immunodeficiency is progressive and associated with 

a high mortality rate (Hinnant et al, 1986). However, antiviral therapies 

have recently become available to fieat patients. 

a- Ganciclovir 

Ganciclovir a nucleoside analog structurally similar to acyclovir, is 

an ffibitor of viral DNA polymerase. Therapy for CMV- colitis is 

associated with weight gain and improved quality of life (Chachoua et al, 

re87). 

Ganciclovir must be glven intravenously and is infused over I hour. 

The usual induction dose is l0 to 15 mdkg per day administered 

2 to 3 

divided doses daily for 3 r,veeks. 

The most frequent toxicities reported with ganciclovir are 

neutropenia, thrombocytopenia, rash, hypotension, ilausea, vomiting, and 

headache, which require discontinuation of the drug or switching to 

alternative therapy in more than 1004 of patients. 

b- Foscarnet 

Foscarnet is an inhibitor of viral DNA polymerases that is active 

lgainsl all the herpes viruses (including CMV) and HIV. Experience is 

limited using foscarnet for the treatment of gastrointestinal CMV disease it 

is given (200 mg/kg per day) by continuous intravenous infusion for 3 

weeks. Syrnptorn resolution and endoscopic healing occurred within 2 

weEks in l5 of l8 patients with esophageal disease and in 15 of 27 patients 

with colitis 

S ide effects of foscarnet, inc luding hypornagn-esemia, hypocalcemia, 

hypophosphatemia, anemia, and renal insufficiency, occur in more than 

20% of patients. Substantial gastrointestinal side effects include nausea, 

vomiting, diarrhea, and abdominal pain. In clinical practice, ganciclovir is 

ugually- the drug of first choice because the risk for renal dysfirnction and 

electolyte disturbances 

much less. 

Conclusions 

Gastrointestinal cMV disease is an increasingly recognized clinical 

problem that occurs in variou settings characterized by impaired host 

immunity. It should be suspected when patients with abnormal immune 

filnction develop symptoms and signs of gastrointestinal mucosal 

ulceration, which is the rnajor macroscopic feaftrre of CMV gastrointestinal 

disease. A diagnosis of CMV in immunodeficient patients can be 

confirmed by identifying cytomegalic cells in mucosal biopsy specimens of 

gastrointestinal lesions. The pathologist can also identifu CMVusing 

special stains for viral markers. 

II- On top qfjnllammalorr bowel disease: 

37

AnalFlgtule 

R*iew of Literature 

Nerohn'S:Xigegg!' 

feafures typical of perianal crohn's disEase are recurrent abscesseso 

fistulae, skin tags ulcers and stricture$ (Crohn, 1960, Fliher et aL, 1976). 

High proportion of fistulae were extra sphincteric or high frans 

sphincteric (Keighhy and Allan 1986). N4ore comrnon in large bowel 

disease particularly with rectal involvernenthan in iliocaecal disease 

(Higgins and Allan, I9E0). 

; 

They are commonly multiple and internal opening is often some 

distant above anorectal ring, The perineal skin is rather indurated with 

edematouskin tags (Keighley, 1993). 

PErianal fistulae occur in 6-340/ of patients with crohn's disease 

(Gilliland and Wexner, 1994. 

Although anal manifestations may bo the initial presentation, intestinal 

involvement follows in many cases (6t'llifcnd and Wexner, 1997). 

B- Ulcerative wlitis: 

f 

Presence ofperianal disease does not exclude ulcerative colitis as they 

are identifiedin 7Yo of patients with ulcerative colitis (Keighley, 1993). 

Most conrmon lesions are fistulae, fissures and abscesses (Buchan 

and Grace, 1973), 

Anal fistulae formation in ulce-rative colitis patients may occur in 

cases with distal proctocolitis or even in segmental forms of colitis in 

which rectum itself remains normal (Goligher et aL, 1984)- 

III-.0n tou of uelvic seusis: 

Rarely, pelvic sepsis from appendicitis, salpingitis, diverticular 

disease, pelvic neoplasm) may result in chrqnic supra levator abscess which 

may either spread caudally in inter muscular sFase to emerge in the 

perineum resulting in high intersphincteric fistulae or may burst through 

the levator ani presenting as an atypical ischiorectal fistulae (Parhs et aL, 

1976). 

B- Traumatic fistnlue 

# 

t 

Trarunatic frstulae develop consequent to increased tissue tension 

devitalization and hematoma forrnation that would initiate the abscess 

fistulae sequencespecially with the higher chances of contamination from 

3t

Anal Flstula 


faeces as 

Either: 

well as complicated apocrine glund secretion in the perineum. 

+ 

* 

l-Complicating penefiating perianal iqiuries due to blunt frauma, stab, 

blast injuriei fAting astride a sharp object or as result sf self 

inboduced foreign bodies anal introduction or swollen chick bones 

or a road traffic accident which usually result in high anal fistulae. 

Z-Complicating operations for anal disorders which may result,l4 

chronic sepsis which later develops fistulae, classically of after 

sclerotherapy for hemonhoidal occasionally after internal 

sphincterotomy. Also following ileal pouch anastomosis after 

parkis mucosal proctectomy and ilio-anal anastomosis. Sphincter 

preserving technique for rectal carcinoma especially trans perineal 

route (Keighley, 199J).Rectal injury following perineal 

prostetectomy (Devin et aL, 1992). Rectal injury following 

posterior colpoperineonaphy (Nerttton and lurain, 198tr). 

Within acquired perineal fistulae post operative fistulae deserve special 

considerations because they have relatively higher spontaneous healing 

rate. Most of them will heal if sepsis and malnutrition are corrected. 

C-Sgrcau$es 

l- Malienanrv 

Not only carcinoma of anal canal but also carcinoma of the rectum can 

cau$e anal fistula by formation of an abscess in one of the perianal tissue 

$pacss and the latter develop into fistula and the malignant tract will not 

heal till all of the disease is removed. 

+ 

Kline et aL, (1964) reported that 44Vo of cancers arising in a fistula in 

ano were colloid in nature 34% were squamous and 25o/o were 

adenocarcinoma. Most of these fumors were inoperable and had spread 

widely into the perineum, buttocks and inguinal lymphatics when they 

eventually presented cliiically. 

There are three main groups of adenocarcinomassociated with 

anorectal sepsis. 

{ 

l- Rectal carcinoma which extend widely in perineal tissues and 

outgrow their blood supply resulting in necrosis and sepsis . These 

have poor prognosis and occur predominantly with elderly so it is 

therefore important to biopsy any suspicious abscess fistula in 

elderly patient, and perform examination under anaesthesia 

(Keighley, 1993). 

39

Anal Fbtnh 

R*tw olLiteratrre 

2-Tumors that occur in association with an anal fistula which are 

usually slowly growing (GetL et aL, I9EI), 

In some of these cases there is tumor situated proximally in the rectum 

and it has been suggested that tumor cells may be sEeded into the fistula 

(Dukes and Gafivln, 1956). 

The pathology may be colloid or adenoearcinoma. In other cases 

malignant .changes in congenital reduplication and some epidermoid 

carcinomas arise from anal gland (Lee etaL,l9ilI, Zarcn et aL, 1983) the 

pathology may be squamous or basal cell carcinoma. 

# 

3. Rare tumor$ which are associated with hidradenitis suppwativa and 

arise from apocine glands (Thornon and Ahcafian, 1978). Other 

malignant tumors may be associated with anorectal sepsis they 

include carciniods (Grace et aI, IhEZ) and primary lymphoma of 

anorectum (Steele et aL, 1995). 

2- Post irradf$atio nerineal ftstulae. 

There should be perineal wound plus pelvic inadiation these perineal 

fistulae arc conrmon with sphincter preserving $urgery tluough perineal 

route rather than transabdominal approaches to extra rectal neoplasms 

(Saclarides, 1997). 

# 

l-Anal disorders. 

A- Hidradenitisuunqrativa: 

may present in anal canal as fistulae, they are usually submucous or 

subcutaneous due to obstructed, infected apocrine glands. The term 

pyodermal fistulans is used to deseribe this entity. 

B-Aselfi$Eu{s 

may be complicated by short superficial fistulae running from base of 

fissur to hyperrophied anal papilla fftasctr*e,.1964). They are almost 

always midline representing 7% of anorectal fistulae (Marhs and 

Ritchte,I977), 

C- Haemorrhoids 

Sepsis cornplicating a thombosed perianal venous plexus may result 

in subcutaneous or submucous fisfulee. 

* 

t 

40

Anal Fbtula 


PATHOLOGY 

{h 

Fistula: Latin word for Reed, pipe or flute' 

Classical defini+ion is an abnormal communication between two 

epithelial surfaces either lined with epithelium as in congenital fistulae or 

ganulation tissue in other cases (Abscess-Fistulae sequence. 

+ 

Classiflcation 

The most widely used system is that of Parks et al., (1976). They 

divided them into 4 grouPs 

l- Intersphincteric 

2- Trans sphincteric 

3- Suprasphincteric 

4- Extra sphincteric, 

+ 

The disadvantage of this classification is the lack of the description of 

the secondary tracks and circumferential spread if present. Horizontal and 

vertical tracks 

A'Yetlicg!^lrqgks Classified as : 

* 

l-tntersphicteric if the track lies between internal and external sphincter. 

2-Transsphincteric if the track crosses the EAS on its path from anus to 

the perinettnr 

3-Suprasphincteric start in the intersphincteric plane and extend upwards 

into sgpralevator compartment where they can break through the 

4l

AnalFlnula 

R*iew otLiterature 

levator diaphragm into ischiorectal fossa discharging into the 

perineum. 

4-Extrasphincteric fistula. Commonly refered to as high fistula which 

lies outside EAS in isciorectal fossa extends high up entering the 

rectum above anoreotal ring. 

* 

B- H o rizo nlsl tt a:c lts : 

Fistulae with external opening ventral to transverse anal line drain 

directly into the anus at dentate line while those with an external opening 

dorsal to transverse anal line take a ctwed course to reach the posterior 

wall of anal canal in midline (Good sall, 1990), 

* 

There are many exceptions for this rule, posteriorly the principle 

exception is the very low fistula which may follow a direct course. Also 

anterior horse shoe fistulae do occur despite Goodsall's rule. Posterior 

horseshoe fistulab are often associated with numerous external opening+ 

particularly when the fistula lies in ischiorectal fossa (Held et al.'1986). 

The surgeon who as$Ess the circumferential spread must thErefore take 

into consideration the sites of intemal and ,extemal opcning and the plane 

of spread which may be intersphincteric ,ischiorectal or supralwator. 

+ 

Horseshoe component occurs in 9o/o of anorectal fistula (Marhs and 

Ritthie, 1977). 

* 

Circr-rmferential spread was most sommon in ischiorectal fossa 

secondary to trans-sphincteric fi stula. 

42

AnalFbtula 

Revlew of Literature 

Circumferential spread in the intersphincteric plan'e may be associated 

with all types of fistulae. 

t. 

Supra levator horse shoe extensions were the least sommon and were 

usually associated with suprasphincteric or extrasphincteric fisfulae 

(Keighley, 1993). 

Internal onening 

t 

Number: it is usually not more than one which is considered the 

prirnary opening but rarely several crypts can be affected and in this case 

they are connected with each other by submucosal or subcutaneous tracks 

secondary internal openings in the anal canal or the recftm are rare. 

Site: it is usually at level of dentate line rarely higher in high anal 

fistulae usually in about 50% or rnore they were posterior next anterior 

rarely lateral (Marks and Ritchie, 1977) (Shoulb et aL, 1986). 

+ 

rh 

The track: 

As any track following an inflamrnatory lesion the lining of the wall is 

composed of granulation tissue developing later into fibrous tissue the 

inner layer of mesothelial tissue will spread on the surface in the form of 

one layer of flattened cells this layer will be replaced later by stratified 

squaxnous epithelium. derived from creeping edge of skin of the perianal 

region. underneath this wall the tissue show the chronic inflammatory 

reaction and, or show specific reaction related to the original causative 

factor. 

43

AnalFbtula 

Revlew olLiteratare 

INCIDENCE 

In a review of 400 fistulae by Parks and associates. The distribution 

r Inter-sFhincteric 45% 

* 

r Trans-sphincteric 30% 

" Supra-sphincteric 20V, 

r Extra-sphincteric 5%. 

Because of the highly selected patient population in this series, Parks 

estimated that a more rspresentative incidence in general population would 

' b e # 

Intersphincteric 70% 

Trans-sphincteric 21% 

Supra sphincieric 5V" 

Extra-sphincteric 7% 

In study on 163 patients by Vasilevsky and Gordon, 1984, the 

distribution was 

Inter-sphincteric 4l% 

Trans-sphincteric 53% 

Supra-sphincteric 3% 

Extra-sphincteric 0 

Multiple 3%. 

* 

*

Anal Fbtula 

Revlew ofLiterature 

SUBDIVISIONS OF FISTULAE 

r 

Interuuhincteric Fistula 

Simnle (Fig.l2a) 

The simple intersphincteric fistula has its internal opening sites at the 

anal valve. The track passes tluough the intemal sphincter to the site of the 

infected anal gland and hence dorvnward in the intersphincteric plane to 

emerge in the perineal region. 

t. 

Simnle witlt Closed external Onenins and Abscess (Fig.lzb) 

If drainage of a simple track is inadequate or the external opening 

becomes occlude, recurrent perineal abscess will develop until the fistulae 

is laid open. 

* 

* 

Hiqh Blind Track (Fig.l2c) 

A secondary track runs upward in the intersphincteric plane to the 

pararectal region but doesn't enter the rectum and is not associated with an 

abscess. 

Hish Track Enterine the Rectum (Fig.l2d) 

+ enters the recturn. 

A secondary track extends upw'ards in the intersphineteric plane and 

45

Anal Fbtuh 

Reviev oJLiteralure 

Hish Track and a Suurelevator Ahscess: (Fipl2a) 

The secondary track passes upwards and ends in a supralevator 

abscess. It is important of this abscessince treahnent involves lying open 

the entire fistula by dividine the internal sphincter and draining the abscess 

into the rectum. Any attempt to drain the abscess througlr the perineum will 

result in a suprasphincteric fistula. 

f 

Hiqh Blind Track and Suuralevator Abscess Without a Perianal 

Openins (Fig.l2f ) 

The lower intersphinctericomponent of the fistula may be absent. 

Hence run$ upward from the dentate line to the abscess in the 

intersphincteric plane. These abscesses drain inef;ficiently because of the 

continued activity of the intemal anal sphincter. There may be a horseshoe 

component. 

# 

Hish Track' Enterine the Rectum Without a Perineal Ouenins 

(Fig.l29) 

Along, high, intersphincteric fistula is found, it has no external 

opening, 

fr 

f 

46

Anal Fbtula 


Fig. (12): Intersphinfieric fistula. (a) R simple intersphincteric fistula 

running from the dentate rine to the rower- border of the anar canar. (b) 

simple 

A 

fistura compricated with a smat perianar abscess and a crosed 

external opening. c) an intersphin*eric fistura with a high brind track 

the intersphincteric 

in 

plane. D) en intersphincteric fistula with a high blind 

track which opens into the rectum. E) an intersphincteric fistura with 

high 

a 

brind track compricated by a supra levator abscess (F) 

intersphincteric 

An 

with a crosed distar end, a high intersphincteric track, and 

an extrarectar abscess (g) A high intersphincteric fistura with a crose distar 

end opening into the recnrm.

AnalFlrtula 


Transrhincteric Fietula 

Simnle(Fig.13 a.b.c) 

The uncomplicated ffans-sphincteric fistula is not a homogenous 

entity. The fistulous track may enter the anal canal at a high or a low level. 

More importantly, the track itself may nearly pierce the lower fibers of the 

external sphincter at the point where one the fibrous septa traverses the 

muscle (low rans-sphincteric). Alternatively, the hack may follow one of 

the venous channels directly ttrough the extemal sphincter opposite its 

internal opening at the pectinate line to enter the ischiorectai fossa., 

discharging into the buttock (mid-trans-sphincteric). Finally, the track 

which pierces the External sphincter may bass dangorously close to the 

anorectal ring before it enters the ischiorectal fossa and the perineum (hrghtrai'rs-sphincteri 

c). 

*- 

f. 

Iltithout Feri\nal Onenins and Recufrcnt ahscess (Fig,l3d) 

Sornetimes the exit track becomes occluded but if the external 

opening remains closed a recurrent ischiorectal-abscess 

inevitable. 

Hish Blind Track: (Fig.l3e) 

This is a coilunon and potentially dangerousituation* The secondary 

ffack may be iatrogenic following enthusiasticurettage of an ischiorectal 

abscess during drainage. Alternatively, it may represent inadequate 

drainage from the apex of, the ischiorectal fossa which, in some eases, may 

be due to a supralevator component. Instead of the track running straight 

from the anal canal throHgh the sphincters to the perineum, a secondary 

track runs up to the apex of the ischiorectal fossa and, in some cases, it may 

extend above the levator ani. 

* 

*

Anal Fbtula . Rlitw of Literature 

The danger of this fistula is that an externally placed probe will tend 

to follow the secondary track and the inexperienced srugeon may push the 

il 

probe into the rectum, thus creating an exfra-sphinoteric fistula. 

Hence it is always .advisable to pass probes refrogradely, first 

searching for the internal opening. Which'provides the clue to the conect 

assessment of the fistula. The technique of fistulectomy has much to 

recommend it in these complex fistulae with secondary tracks may be 

accurately defined. 

+ 

Hiqh Blind Track With Sunralevator Abscess: (Fig,l3f) 

This is arrother potentially dangerousituation unless the primary 

trans-sphincteric fistula and the secondary translevator track are accurately 

identified. If the supralevator abscess is incorrectly assumed to be an 

intersphincteric fistula and drained into the rectutn, the surgeon will have 

created an extrasphincteric fistula. 

t' 

fr 

49

Anal Fbtula 


I 

t 

* 

Fig. 13: Trans-sphincreric fistula a) a low lying trans-sphincteric fistura b) 

High trans-sphincteric fistura associated with ischiorectar abscess c)Mid 

trans-sphincteric fishrla with an intersphincteric abscess d) Mid trans_ 

sphincteric fistula with a crosed distar end compricated by an ischiorectal 

and an intersphincteric abscess e)Mid trans-sphincteric fistura compricated 

by a high blind track and a high ischiorectal abscess f) Mid transsphincteric 

fistula complicared by a high brind cuhninating in a 

supralevator abscess 

3 

+ 

50

Anal Flstula 

Review afLiterature 

il 

Sunrasuhincteric Fistula 

Simnle (Fig.l4a) 

Suprasphincteric fistulas are common than most people generally 

appreciate and they are amenable to conservative surgical treafinent. Most 

fistulas are due to suprasphincteric abscess complicating an intersphincteric 

fistula that bursts through the levator ani into the ischiorectal fossa to 

discharge into the perineum. The fistula track starts in the intersphincteric 

plane and loops over the puporectalis and external sphincter complex. 

* 

With Suopralevntor Extension and Abscess: (Fig.lab) 

The presence of a supralevator abscess nearly reinforces the common 

etiolory of this fistula. The supralevator collection often spreads zuound the 

anorechrm and there is commonly a high horseshoe component. 

h 

* 

Fig l4: Suprasphincteric fistula (a) Simple suprasphincteric fistula b) 

Suprasphincteric fistula complicated by a suprasphincteric abscess. 

Extrasnhincteric Fistula : 

It mnst be admitted that the majority of extrasphincteric fistulas are 

iatrogenic, but forlunately the are rare. In the experience of Abcarian and 

5l

Anal Fbtula 

Revi*v of Literature 

- 

colleagues they occurred in less than 3% of patients admitted to a specialist 

center (Ai:tcarian et aL, 1987) If there is no history of surgical interference 

most exti,nphincteric fisfulas are due to a pelvic abscess caused by rectal or 

gynecological disease which has penetrate the pelvic diapluagm and 

dischargeri tluough the buttock. This is a particularly common situation in 

Chron's disease or following penetrating injuries (Abcrian et al., 1gS7), 

I 

Unfortunately, rnost remaining extrasphincteric fistulas are due to 

overenthusrastic drainage of an ischiorectal abscess, when the rectal wall is 

inadvertently darnaged (Fig lSa), or as result of rectal injuries, surgical 

damage to the rechlm, drainage of supralevator abscess secondary to 

transsphinctelic fistula into the rsctum, or the passage of a probe through a 

high seconciarlr track complicating transsphincteric fistula. (Fig.I5) 

.; 

il 

Fig. l5: Extrasphincteric fistula a) Extrasphincteric fistula due to iatrogenic 

damage to the rectum during drainage of an ischiorectal abscess. b) 

Extrasphincteric fi stula complicating a trans-sphincteric fi stula damage. 

# 

52

Anal Fhtula 

Materials & Methods 

MATERIAL AND METHODS 

I 

Material: 

Most of this work was derived from patients coming to out patient 

clinics of Kasr-El-Aini hospital complaining of discharging fistulae in 

perianal region. 

All sases were examined acconiing to the following sheet. 

A- oersonal historv 

* 

Name Age Sex 

Address occupation Admission date 

B- Camplaint 

* 

+ 

C- Historv 

Pnrritis 

Peri anal discharge 

Abscess (swelling in perianal region) 

. l. Diseases: 

- Incised - Burst 

Bilharziasis, T.8., Malignaney, Diabetes, AIDS, 

and any other disease. 

2- Previousurserv for anal fistula 

53

Anal Fhnrla 

Materials &Mcthods 

D- Examination 

General: chest, AHomen 

Local: anal, perineal 

Instrumentation: Anoscope 

* 

E- Lahor atorv investisations : 

CBC LFT Renal functions 

F.B.S. 

Cytomegalo vinrs antibodies 

IeG 

- tgM 

F- Imapins of fritulous track (if neededl. 

Fistulogranr 

Trans rectal endosonography 

CT 

MRI 

t 

G- Qoeration: 

Date 

Findings 

. Procedure 

- Fistuleotomy Fistulotomy 

t 

# 

54

Anal Fbtula 

Matefials & Methods 

H- P atln lo sical examinatio n 

t 

of biopsy taken during surgery in search of specific pathology using 

two methods 

l- Routine llx. and oesin looking for glanulomas or inclusion bodies. 

2- lmmunohistochemicai staining for presense of CMV 

I- Short term follow un 

. for 6 to 9 months to detect early recurrencE 

l[ 

J* Statisticul evalaation of resalts. 

# 

* 

55

AnalFbtula 


Methods: 

| -Throus h hktorv tqkins: 

* 

The residence for endemicity of Bilharziasis 

Anal complaint especially asking about 

. Development of abscess in perianal region and if the latter had 

been incised or was left to brust and since whEn. 

. Previous operations for anal fistulae and degree ofcontinence. 

History of 

. different specific diseases e.g. Bilharziasis, T.B.*-*--etc. 

r Debilitating disease that lowers the immunity e.g. malignancy, 

# 

AIDs, DM.,... etc. 

. Inflamrnatory bowel disease.g. Crohn's , ulcerative colitis 

2- Genernl Examination 

For presence of: 

T.B.: tuberculous nodes in neck or pulmonary T.B. 

* 

Bilharziasis: Hepatosplenomegaly, ascites. 

Amoebiasis: palpable tender spastic sigmoid or caecum. 

fi 

56

AnalFbula 

Materials &, Methods 

3- Local examinatio& 

ft 

a- Inspection of nerranal reeionJor 

1- External oneninos 

Siie: Anterior Right or left 

number 

Distance from artal verge 

Appearance 

- on summit of raised area formed of granulation tissue 

- lnconspicuous and only detected by passage of pus on 

pressure 

11 

- With bluish undermined edge with thin watery yellowish, 

discharge characteristic of TB 

2- The re:;l o/'flerianal resion fbr 

- Evidence of pruritis 

Discharge from anal' orifice. 

- Any associated anal condition 

rl 

+ 

Externalpiles, 

sentinel pile denoting fissure, 

- scar of any previous operative interference for fisfula or 

abscess. 

B- Palpation of perianal resiqn 

- Induration along track. 

* Presence of any collection 

- to detect site of extenral opening by applying pressure on 

track. 

5'l

Anal Flrtuli . 

Materials & Melhods 

C- Per rectal examination to detect 

- Tone of sphincters 

- Site of intemal opcning felt as depression dimple or on 

raised papilla. 

rr 

- Relation of site of intemal opening to pectinate line and 

anorectal ring. 

- Any associated lesion 

. ckonic fisstue 

Detect intersphirrcteric or supralevator abscess and 

$trichre in lower rectum and 

polypi or masses 

- Discharge on examining finger denoting proctitis. 

* 

' 

D- Bimanual examination to detect fistulae secondary to pelvic patholory 

4- I nstru mentation Anosco0v : 

Illuminated proctoscope could demonstrate 

' 

Site of internal opening and any discharge coming from it. 

r Edematous crypt or enlarged papilla denoting cryptitis 

f 

r Amoebic ulcers with nonnal intervening muaous membrane. 

r Any associated lesion Internal piles, masses or polypi. 

* 

5E

Anal fbtula 

Materlals & Methods 

* 

5- Inve#tigation 

A- Laboratorv 

. CBC 

Eosinophilia favoring parasitic infestation 

Leukopenia with relative lymphocytosis tuberculous infection. 

r F.B.S. for DiabEtic patients 

. Serology for cytomegalovirus by detection of cytomegalovirus anti 

bodies in sera IgG, IgM. 

B- Radioloqisal if needed 

* 

L [.'istulosranhv By which we can determine 

+ 

r Course of fistulous track especially in cases presenting with multiple 

external openings 

r Direction of track and its side branches and whether it is high or low. 

O Presence ofinternal opening or nol 

r Method: Tlrough injection of lipiodol through one of the external 

openings and an anteroposterior view in addition to oblique or lateral 

view were taken during injection. 

z-frans rectalultra 

By which we can determine 

* 

. Presence of collection i,e. abscess cavity and its site 

. Presence oftracks and their course, branches 

. Relation to sphincter and site of crossing of sphincter if present. 

. Relation to levator muscle infra or supra levator. 

59

AnalFhtula 

Matertals & Methods 

r Intersphincteric fiack is seen as hypoechoic line nrnning through the 

normal hlperechoic longitudinal smooth muscles 

r Trans sphincteric Extension was identified by hypoechoic line 

extending tluough external sphincter outwards 

* 

3- CT examination 

It may show supralevator absces$, extent of perirectal or perianal 

fistula, connections to adjacent viscera (Yousem et al., l98l). 

Disadvantage 

l-Fistulae may be mistaken for inflammation of muscles. 

2- Coronal imaging of anorectum with C.T: is unsatisfactory exact site 

of fistula related to levator complex is poorly shovm in an axial 

C.T, images (Guilkrumin et al., 1986), 

t 

4- M.R.I. 

_ 

In recurent cases with diflicult assessment by examination and 

routine investigation may give better assessment to Course and bnanches 

and site of intornal opening, abscess and relation to levator and anal 

sphincter can be displayed preeisely. 

t 

Fibrotic process by repeated operatiorts can be demonstrated and 

fistulous disease can be clearly differentiated from it (spencer et aL,I998). * 

60

AnalFbtula 


* 

Saline instillation in the anal fistula causes distension of the collapsed 

walls and filling of the dry ffacks, abscess cavities and secondary 

extension. 

The advantages of utilizing saline as a conEast material in MRI 

fistulography 

that it is harmless and inexpensive (Myhr et aL, 1994). 

6- Onerative findinEs 

+ 

I.Pnor to sureical 

while on table for better assessment probing may be done: 

A probe pointed guide made of malleable alloy was passed through 

external opening very gently to avoid false passage and a finger introduced 

in anal canal to judge direction and depth of track. Then using anoscopy the 

probe could pass to lumen tluough internal opening 

II durinq strreical procedure 

. bener description of the track, its relation to sphincter muscleside 

* . 

branches and level of internal opening was done. The 29 cases were 

grouped according to the types of fistulae at end of operative exploration 

into 2 groups 

Group A intersphincteric fistulae: 24 cases 

.* Group B transsphincteric fistulae: 5 cases 

6l

Anal Fbtuh 


7- Patholosical sndv of the fiack 

The tissues removed during operation of fistulectomy or fistulotomy 

were fixed in l0% neufral formalin solution for 24 hours. Processing into 

paraffin was performed by the standard histopatholory laboratory method. 

The histologlc sections prepared fiom the paraffin blocks were cut 4-5 

miqrons in thickness and strained with haematoxylin and Eosin for routine 

histopathological examination. Another histologic section from each case 

was also stained immuno histochemically for the presence of C.M.V. 

# 

C.M.V. immunostaininq 

Principle: lrr this study the Biotin-Streptavidin Amplified (B-Sa) 

system was applied. In this system tluee reagents are utilized: the frrst is 

the primary antibody specific for the antigen to be localized. The second 

reagent is the biotinylated secondary antibody which is capable of 

bounding to both the primary antibody and the label acting as efficient link 

between them. The link provides additional steps for amplification of the 

antigen binding event. The third reagent or the label is composed of 

peroxidase-labeled streptavidin with a carrier protein. Visualization of the 

antigerr/antibody reastion is dependent on the ability to produce an 

insoluble coloured product at the site of the reaction by atr appropriate 

chromogen. 

Steps of Staining 

"* 

t 

# 

I- Paraffin blocks were cut by a microtome at 3-4 micron thickness. 

Paraffin sections were picked up onto poly"lysine coated rnicroscope 

62

Anal Flstula 


t 

slides and dried ovemight at room temperafure. A circle was drawn 

on the slide around the section by a diamond pencil to rnark the 

surface of the slide. 

2- Slides wers put in xylene overnight to ensure proper 

deparaffinization, then the 

decreasing concentrations of alcohol to water. 

slides were rehydrated through 

* 

t 

3- Antigen retrieval by microwave pretreatment: For demonsfratjon of 

. C.M.V. antigen, endogenous peroxidase activity was blocked using a 

3% solution of hydrogen peroxide in methanol for 30 minutes (mins) 

at. room temperature. Slides were washed well in water beforE 

immersion in 200 ml of l0 mM citric acid adjusted to pH6 with 2N 

NaOH> Slides were then microwaved on high power for 5 mins 

(Goldstar 1000 Watts with digital control), removed and topped up 

to the original level with distilled water. The previous step in this 

case was repeated twice as it depends on fixation and the antigen 

being dernonstrated. Slides were removed fronr the microwave and 

left to stand for l0 mins at room temperahrre before being washed 

well in nrnning tap water then in phosphate buffered saline (PBS) for 

5 mins 

-+ 

4- Excess buffer was blotted off and slides were then dried except for 

the tissue sections using absorbent paper. 

5- One or two drops of the supersensitive ready-to- use monoclonal 

antibody to CMV antigen(Dako) were put on the tissue sections. 

63

Anal Fbtuh 


G 

Slides were then incuhated horizontally in a humid chanrber at room 

temperature for 120 mins. 

Slides were washed three times in PBS. 

# 

7- 

Biotinylated (antimouse) secondary antibody was added and 

incubated for 20 mins at room temperature. Slides were then washed 

in PBS as before. 

8- 

One or two drops of label avidin-biotin complex (ABC) were applied 

for 20 mins at roorn temperatr.re then sections were washed in PBS 

as before. 

* 

9- Colour was developed using diaminobeneidine (DAB) which was 

applied for l0-20 mins. Slides were then rvashed in water for Smins. 

l0- Counterstaining was done using Mayer's haematoxyline 

(Dako).Slides were then washed in water for 5 mins 

ll- Slides were dehydrated through increasing concentrations of ethanol 

then cleared with xylene. 

I 

12- A drop of Canada balsam mountant was added and sections were 

covered by a glass cover. 

# 

Controls: 3 cases of placental tissue infected with the virus were used 

as a positive control, As a negative control, a tumor tissue section was 

processed in the above mentioned seguence but the primary antibody was 

(t4

Anal Fhtula 


t 

not added and PBS was used instead. Phosphate buffered saline solution: 

7.75 gNacl 0.?0g monobasic and 1.5g dibasic potassium phosphate 

Adjusted to pH 7.6 

I Short terry follow up 

- for 6 to 9 months to detect earlv recurrence 

I Statisticul evaluation 

was done usirrg Kruskal-Wallis one way non paralnetric AOV. The 

significant level when P is < 0.05 

* 

* 

t 

65

Anal Fbtula 

Re,yu/fs 

RESULTS 

t 

This study was conducted on 29 patients presenting with anal fistulae 

in Kasr El Aini hospital. 

Patients were Erouped according to the types of fistulae at the end of 

operativ exploration into two groups: 

l-Group A: 24 patients with intersphincteric fistulae. 

Z-GroupB: Spatients with trans-sphincteric frstulae 

TF 

Group A was fruther divided into 

a- fissure fistulae: 

6 cases 

b- Low intersphincteric: Tcases 

c- Complex fistulae: 

I lcases 

Table:3 Showing Distibution of cases according to classification of Park's 

+ 

for anal fistula 

Type of fistulae 

Nrunber of cases 

Intersphincteric 24 

Fisswe fistulae 6 

low intersphincteric 7 

*, 

complex 

Trans-sphincteric 5 

Extra-sphincteric 0 

Supra-sphincteric 0 

I I 

66

Anal Flstula 

rte,nr/rs 

A* preoperative work up included: 

l- Demographic studies 

Grourp A: ?l males and 3 females t 

Group B: 5 males and no females 

?- Laboratory serologic studies: 

Group A: Positive cytomegalovirus IeG antiUdAy in serum was 

detected in 14 patients whereas it was negative in one case 

Group B: positive cytomegalovirus Igff antihody in senrm was 

detected in the 4 cases tested in this group. 

* 

Table 4: showing results of laboratory serological studies in the group 

Group A 

fissue fistulae 

under studv 

low anal fistulae 

complex fistulae 

CMV IgG 

antibody 

positive in serum 

CMV IeS antibody 

negative in seruur 

Group B 4 0 

3 

4 

7 

0 

0 

I 

Not tested 

3 

3 

3 

'} 

# 

61

f-- 

I I 

fe.vlts 

3-Imaging studies were 

AfistulograPhY was done in 4 cases 

t 

L 

I 

I 

lil 

I 

I 

II 

l}, 

Fig. 16: showing fistulography of case 5, showing high perianal 

fistula 

I

Re.fl/fts 

B- Endoanal sonography was done in l0 cases: 

il 

Fig 17: Fistulous hack at right anterolateral aspect in intersphincteric 

plane with no side branches crossing muscle complex 

} 

] 

Fig l8: Fistulous track at right anterolateral aspect in transsphincteric 

plane reaching up to level of levator but not above. No abscess cavities 

t 

69

.Resu/ts 

+ 

MRI was done in one case 

t 

I 

+ 

no pelvic collection cor-rld be detected 

7(l

Analtktula 

Re.flrlts 

4- At operation: the fistulae were classified according to the findings 

during dissection ihto: 

a) Group A: 24 patients with intersphiucteric abscess fistulae * 

sequsnoe. They were firrther divided into 

a- fissrrre fisfulae: 6 cases 

b- low intersphincteric simple: Tcases 

c- Complex fistulae : I I cases the problems with these fistulae were: 

. Intersphincteric with an internal opening at 

dentate line and a high blind track6 cases 

. Intersphincteric with infralevator abscess and side 

branches 3case 

* 

' lntersphincteric with $upra levator abscess 2 

cases 

b) Group B: S"patients with transsphincteric fistulae. 

According to intenral opening: 

ffrc c&s€ had an internal opening at ttre dentate line 

s 

Four cases had ur opening above the dentate line 2 of 

which had supra levator detectable internal opening 

b* Postoperative work up included 

il 

l- Hx and eosirr studies were negative in all cases as regards the 

pre$ence of any specifrc granuloma or histologically detectable inclusion 

bodies 

7l

Re.ru/ts 

+ 

* 

Fig 20:The stratified squamous epithelium adjacento a fistulous fract 

showing mild epithelial hperplasia with focal koiloaytosis (H & E x 40) 

t 

+ 

Fig 2l: A fishrlous fiact lined by septic granulation tissue with few giant 

cells(H&E xl00) 

72

.Resu//s 

I 

+ 

Fig 22: High power of the previou$ case showing 2 giant cells surrounded 

by many inflammatory cells (H & E x 400) 

|} 

f 

Fig 23: Another giant cell surrounded by many inflammatory cells (H & E 

x 400). 

# 

73

Anal Fbtula 

Z-Immunohistochemical staining for detection of cytomegalovirus 

antigen were done in all cases 

* 

It revealed positive cytomegalovirus antigens detected in 7 cases 

ilmong 29 cases 3 of the positive cases had both nuclear ani cytoplasmic 

positive staining. I of the positive cases had only positive nuclear staining 

and the last 3 positive cases had only positive cytoplasmic staining. 

The cytomegalovirus positive cells were cells detected at squirmous 

epithelium at the internal opening of fistulae not within the fistulous fiacks 

themselves. 

* 

it 

+ 

74

tesz/rl 

I 

I 

t 

Fig 24: An immuno$taining for 

epithelium 

cMv 

adjacent 

fl3wins 

negative 

to the fistula 

staining 

(pApx of 

a0) 

the 

1) 

I 

for CMV showing positive staining of the + 

75

Resu/ls 

+ 

* 

Fis 26: An immunostaining for CMV showing positive staining of the 

ep*ithelium (PAP x 40) 

I 

\ 

III 

Fig 27. An immunostarning for CMV showing positive staining of the 

cytoplasmio *O nu"t*ut 'tultting of the epithelial cells (PAP x 100) 

'16

Resrlts 

# 

Fig 28: An immunostaining for cMv showing positirre -'- 

nuclear 

cytoprasmic -.r 

staining 

and 

of the epithelial cells (pAp x ldOj 

} 

T 

Fig ?9: An immunostaining for CMV 

staining of the epithetial ceils (pAp x 400) 

showing positive cytoplasmic #

Resn/ls 

t 

t 

Fis 30: An immunostaining for CMV showing positive nuclear staining of 

thJ epithelial cells (PAP x a00) 

t. 

t 

Fis 3l: An immunostaining for CMV showing positive nuclear staining of 

thl epittretial cells (PAP x 400)

Anal Fbtula 

.Rcsulrs 

The disfribution of cytomegalovirus positive cases in the group under 

study is shown in table (5) 

Table 5: Showing thc distibution of positive cases with cytomegaloviru, 

detected in the pathological specimen of their fistulae 

il 

Group A 

A Fissure fistula, 

B Low anal fistulae 

c-Complex 

CMV positive cells 

4 

2 

I 

CMV ncgative cells 

Group B 0 5 

2 

f 

l0 

f 

Statistical analysis within the intersphincteric fistulae group revealed a 

statistic.ally significant relation between Iow anal fistulae and the presence 

of evidence of cytomegalovirus antigen (P=0,0465). 

Furthermore Chi-squared analysis within the same group revealed a 

statistically signifieant relation betwqen fissure fistulae and presence of 

evidence of cytomegalovirus antigens (F = 0.044) 

f 

c- Shorterm follow up for 6-9 months 

It has revealed the presence of recurrence in 7 cases The distribution 

of the cases with early recurrence is shown in table (6) 

F

AnalFlstuh 

Refllls 

Table (6) Showing distributions of postoperative recurrent cases within the 

studied Soup. 

f 

Group A 

a-Fissure fistulae 

b-Low intersphincteric 

c-Complex fistnlae 

No detectable 

) 

7 

6 

recuJTences 

Group B ) 0 

Postoperative 

I 

I 

5 

rscurTences 

s 

t 

Further study of these recuffent caseshows 

a- 5 cases from the I I cases of complex intersphincteric fistulae z of 

them had supralevator abscess 3 of them had high blind nack 

b- I case from I cases of low intersphincteric simpre fistulae 

recurrence seemed to be related to a stitch in the repair or it may 

be missed blind track 

c- I case frorn 6 cases of fissure fistulae, recurrence in the form of an 

abscess related to tlre scar. No detectable fisnrlous track up till 

now. 

.il 

d- only one case among 7 recunent cases had evidence of positive 

cytomegalovirus antigens. It was the recurrent case of fisswe 

fistulae 

statistical analysis within the intersphincteric fistulae goup 

revealed no statistically significant relation between recurrence 

and presence of positive cytomegalovirus antigens. 

EO

Anal Fbtula 

DJscussion 

DISCUSSION 

s 

More reputations have been damaged by the unsuccessful treatment of 

fistula-in-ano than bv excision of the rectum. 

The notoriety of anal fistula led Salmon (who operated on Dickens for 

the condition) to found St. Marks hospital in 1835 for the treaftnent of 

fistula and other disease of the rectum (Lattimer et aI., 1996). 

Fistulae-in-ano have an unenviable reputation for recurence and 

compromised continen ce (Keighley, I 993). 

f 

Several factors have been listed ts predispose for recurrence followrng 

treatment of anal fistulae, these factors may be related to peculiarities of 

anatomy of the region (poor drainage of certain spaces), to pathological 

surprises or finally to iatrogenic intra or postoperative mishaps. 

# 

Pathological surprises as the presence of primary pathogens, or 

malignancy, may be a factor wofth of more consideration. 

Three factors inspired the launching of this study- 

First: the frequent recurrence rate despite seemingly adequate surgical 

* intervention for anal fistulae reported in literature. 

Second. the frequently reported non-specific pathology of the 

pathological specirnens: which may reflect lack of diligent pathological 

tl

Anal Fbtuta 

Dlsqtsslon 

search for virar infections beyond flre limit of the routine 

histological 

Hx. and 

assessment. 

eosin 

Third: the report of Tang et aL, (lggs) of the first 

coritis 

case of 

compricated 

c.M.v. 

{ 

by perianar fistura formation in a patient 

evidence with 

of imrnunocompromise. 

no 

This report sfimurated the 

search 

authors 

for the 

to 

rore of specific pathog*ns in anar fisturae 

cytomegalovirus. 

especially 

patients under study were 2g consecutive patients presenting 

fisfulae. 

with 

There 

anar 

was no contrors because we were not sure 

specific 

of 

pathorogy 

finding any 

in the specimens excised from these prttients. 

t 

The patients were grouped accordin g to park,s (Ig,6)crassification: 

into intersphincteric, transsphincteric, exfia sphincteric 

suprasphincteric 

and 

fisturae, however in this series we had 

categories 

the first 

of patients. 

two 

Being the more comnro* gpes to present in generar. 

This crassification was based on the intra-operative diagrcsis 

clinical not 

or imaging 

on 

findings. Hoping that intra+perative 

gold diagnosis * 

standard, 

is the 

that should be checked onry by the incidence 

recunence 

of 

(may 

early 

be it was a misdiagnosis). 

Immunohistochemicar 

studies were chosen for identification 

c'M'v' antigens of 

because of rrigher sensitivity t 

of detection 

conventionar 

compared to 

Hx and EOsin studies and virar curfures 

specimens 

ftom mucosar 

(Goodgame, IggJ). 

82

Anal Fl$tula 

Dr'scusslon 

t 

Serum Cytomegalovirus IgG has been positive in the majority of 

patients under study, with no positive cases for conesponding IgM 

antibody i.e, nothing suggestive of recent infection. However in view of the 

high prevalence of IgG anti C.M.V. antibodies in most adults, this assay is 

not helpful as a diagnostic tool to detect C.M.V. disease. However both 

antibodies do'. not estahlish the diagnosis of tissue-invasive disease 

(Goodgame, 1993). 

TF 

Clinically all patients under study had no symptom suggestive of 

cluonic colonic patholory and their general and abdominal examinations 

were urevealing of any detcctable pathological findings to be associated 

with local rectal examination findings. 

' 

The results of study revealed 24 patients having an intersphincteric 

t 

t 

fistula with the rest of patients having transsphincteric fistulae, which is 

sirnilar to the incidence 

rnore extedsive series of patients. 

Routirre histopathological assessment was negative for detection of 

specific granulomata (e.9. T.B. or Crohn's disease) or inclusion bodies (as 

owl eye of nuclei of cytomegalovirus infections). 

lmu,rrrnohistopathological assessment using monoclonal antibodies for 

C.M.V. lras revealed the presence of positive staining in 7 patients of this 

series. 

E3

Anal Fbtula 

Dlscasslon 

The stained cells were within the squflmous epithelium 

surrounding the internal opening of the ercised fistulae: no positive 

cells were detected within the fistulous tracks as these were mrinly 

lined by 

granulation tissue with surrounding foreign body 

granulomata occasionally. 

# 

This report may be the lirst in literature to describe this finding. 

In fact Roherts et aL, (19,89) reported that columnar surface epithelial 

cells and never squamous epithelium are frequently infected at the edge of 

the gastrointestinal ulceration and in the nearby mucosa that is not 

inflammed in their study of intestinal lesions due to C.M.V. disease. Tung 

et al., (1988) reported cytomegalic cells with prominent intranuclear 

inclusion bodies scattered along the endothelial and epithelial cells in their 

rectal biopsy around the internal opening of their reported fistula (i.e. 

columnar epitheliurn), 

* 

Further study of patients showing positive cytomegalovirus antigen in 

their specirnen revealed that they were mainly in the patients presented 

with intersphincteric fi stula. 

t 

Furthermore statistical analysis within this major subgroup revealed a 

statistically significant association of positive cytornegalovirus antigen in 

patients with low intersphincteric fistulae specially those with fissure 

fistulae. (P:0.04). 

* 

These findings could be a preliminary report needing further 

verification and reusing several speculations. 

t4

Anal Fhtula 

Disczsslon 

* 

Further verification may be tluough staining control specimens of anal 

. and rectal mucosa of patients with no fistulae to check the presence of cells 

positive for cytomegalovirus antigen within these specimens to exclude the 

Further speculations are several: however these are dependant on the 

findings in the suggested control group: first whether the findings of the 

present study is due to cytomegalovirus concomitant infection or the 

fistulae may be manifestation of cytomegalovirus disease.in the anorectum. 

!F 

Until further study is obfained: it may be suggested that 

cytomegalovirus disease may manifest in the anorectum hy a fissure 

fistulae, this may have several backgrounds, 

I 

1S 

First :Herpes simplex (a D.N.A. virus closely related to 

cytomegalovinrs) is knorvn to prodirce painful anal ulcers that may be 

confused with an anal fissure. However, these ulcers are atypically located 

and typically they are more painful than their superfrcial appearance 

suggest (Hicks und Timmeke, I99l). Thus, cytomegalovirus can be 

expected to produce a sirnilar lesion, however it was noticed that in cases 

with fissure fistulae positive for cytomegalovirus antigens, they were not 

as$ociated with marked pain or anal spasm than the conesponding fissrue 

fistulae cases showing negative study for cytomegalovirus antigen. 

Herpes simplex as an infection is known to affect nervous as well as 

mucocutaneous tissues, in fact the vinrs remains dormant in the nervous 

system and thus when infection is activated it is very painftrl. 

Second: cytornegalovirus infection in the G.l.T. has been known to be 

associated with ulceration and sometirnes perforations due to affection of 

85

Anal Fbtula . 

Disctrssion 

the vascular cndothelium as well as tre covering mucosal epithelium. Thus 

Goodgame, A|fi) 

suggested that vascular occlusion may be an important 

cause of tissue injury in C.M.v. disease and thus Zry infection of resulting 

tissue necrosis may lead to an abscess-fistula sequence if c.M.v. leads to 

anal ulcers. 

* 

At the start of this study it was expected that fistulae specimen 

positive for specitic patholory such as cytomegalovirus infection would be 

rnore prone for early recrurenoe. However, analysis of this limited study. 

did not show a statistically significant association between early reourrence 

and positive C.M.v. antigen detection of the excised fistulous specimen, 

This may be explained by the more frequent association of c.M.v. antigen 

positivity and low fistulae especially fissure fistulae, these types of fistulae 

are usually amenable to adequate surgical procedures by frstulotomy or 

fistulectomy with less incidence of early recunence due to premature 

t 

closure of defects with epithelialization of the tracks associated with more 

complex fistulae. 

Finally, C.M.V. detection in fistulae specimen may prove to be higher 

than those reported in the present series due to several considerations: 

A- specimens studied after fistulotomy may not include the internar 

site of opening of fistulous tracks, and thus specimens may show 

false negative results for C.lvt.V. antigens 

B- ln situ D.N.A. probe for C.M.V D.N.A. or polymerase chain 

reaction to identifu C.M.V. D.N.A. in tissues may be even more 

sensitive than immunohistochemical analysis in detection of viral 

antigen. 

tr 

t' 

studies. 

This study is just a preliminary report for further confirming 

B6

Anal Fbtula 

Summary 

SUMMARY 

The aim of this work is to assess the role of specific pathogens 

# especially cytomegalovirus in the pathogenesis of anal fistulae. 

This work was done on 29 patients 

Kasr-El-Aini hospital. ,. . 

fistulae. in 

+ 

' 

A tirll history, clinical exarnination and laboratory investigations 

including CBC, Renal and liver functions were done in all cases in addition 

to detection of Anti c.M.v. antibodies IgG and lglrl in sera of most 

patients 

Imaging of anal fistrrlae was clone in rDlne cases in form of 

fistulography 4 cases, Encloanal ultrasonographl, l0 cases and MRI one 

case which help in proviclirrg sorne inf'ormation about type of fistula and 

presence of collection. 

+ 

A pathological study of excised specimens was done to discover 

presence of pathogens using 

'# 

into 

A Hx. and Eosin staining 

B. Imrnuno histochernical staining to detect c;,tomegalovirus antigens. 

The patients were grouped according to park's (1976) classification 

87

AnalFbtuh 

Sanmm,! 

Group A: Intersphincteric fistulae 

24 cases further subdivided into 

6 cases of fissure fistulae 

7 case simple low anal fistulae 

"fr 

l l cases of complex fistulae 

Group B: Transsphincteric fistulae 

5 Cases 

There was no cases of supra sphincteric or extra sphincteric fistulae 

Routine histopathological exarnination using Hx and eosin was + 

negative for detection of specific pathogens 

However immuno histopathologibal assessment using monoclonal 

antibody for cytornegalovinrs antigens has revealed the presence of positive 

staining in 7 cases. The positive stained cells were within the squamous 

epithelium surrounding tlre intemal opening of the excised fistulae 

All positive cases were mainly in the patients presenting with 

intersphincteric fi stulae. 

Statistical analysis revealed'statistically significant association of 

positive cytomegalovirus antigen in patients with low intersphincteric 

fistula especially those with fissure fistulae. 

fr 

This result could be a preliminary report which need further 

verifi cation and reusing several speculations. 

8E

Anal Fbtula 

Summary 

t 

Further verification may be tkough staining confiol specimens of anal 

and rectal mucosa of patients with no fistulae to check the presence of cells 

positive for cytomegalovirus antigens within these specimens to prove or 

disprove the virus from being primary etiological factor in anal fisnrlae 

Further speculation about the findings of the present study whether . 

due to cytomegalovirus concomitant infection or low fistulae especially 

fissure fistulae, rnay be manifestations of cytomegalovirus disease in the 

ano rectum, 

# 

until further study is obtnined it may be suggested that 

eytomegalovirus disease may manif'est in ano rectum hy low fistulae 

especially fissure fistula . 

Statistical analysis of this study doesn't show 

significant 

association between early recurrence 

cytomegalovirus detected in the excised specimens. 

a statistically 

and positive 

* 

studies. 

This study is just a preriminary report for further confirming 

i 

89

Anal Fktula 

References 

REFERENCES 

Abcnrian, H., Dodi, J., Girona, J., et al., (1987)l Fistula in ano: 

* 

symposium. Int. J. Colorectal Dis;2:51-71. 

Allen, J.T., Silvis, S.E., Sunner, H.W., and McClain,. C.J.,(1981): 

Cytomegalovirus inclusion disease diagnosed endoscopically. Dig. 

Dis. Sci., 26: I33-5. 

Ani, A.N., and Solanke, T.F., (1976): Anal fistula: a review of 82 cases. 

Dis. Colon Rectum: 9:51-55. 

Aqel, N.M,, Tanner, P., Drury, A., Francis, N,D., and Henry, K.,(1991): 

{1 

Cytomegalovirus gastritis with perforation and gastrocolic fishrla 

formation. Histopathology; l 8: I 65-8, 

Arbustini, E-, Grasso, I\{., Diegloli, M., Percivalle, G., Grossi, P., and 

Bramerio, M., et al., (lgg2): Histopathologic and molecular profile 

. of human cytornegalovinrs infections in patients with heart 

transplants. Am. .I. Clin. Path.,98:250-13. 

il Arnaout, H.M. and Abul-Ata, K.A. (19721: The role of Bilharziasis in the 

pathogenesis of anal fishrla Kasr-El-Aini J. Surg., l3:253. 

ot- 

l-l:l; 

of the externar sphincter 

man Acta 

llliJ:Anatorrtv 

* Balthazar, 8.J., Megiborv, A.J., Fazzini, E., Opulencia, J.F., and Engel, 

L (1985): Cytomegalovinrs colitis in AIDS: radiographic findings in 

I I patients. Radiology; 155:585-9. 

90

AnalFlrtula 

Relervnws 

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A CLINICO.PATHOLOGICAL STUDY OF ANAL FISTULAE

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