The colon

Anatomy. This can be distinguished from small bowel by its sacculated structure, and
by the presence of taenia coli and appendices epiploicae.

The cecum, the transverse colon, the pelvic colon are completely cowered with
peritoneum.

The ascending colon, the right colic flexure, the left colic (splenic) flexure, the
descending colon are covered by peritoneum only on its front and sides and are fixed in
position.

Arteries of the colon: the ileocolic and right colic arteries, the middle colic arteries
- all branches of the superior mesenteric.

The upper and lower left colic (sigmoid) arteries, from the inferior mesenteric.
Between these arteries there is a free anastomosis by marginal vessels lying close to
the bowel.

Lymphatic drainage of the colon. This is of great importance in regard to the

spread of carcinoma. Glands draining the colon fall into four main groups - epicolic
glands lying on the surface of the bowel wall; paracolic glands between the layers of
the meso - colon close alongside the bowel; intermediate glands along the branches of
the mesenteric arteries; and central or principal glands around the main trunks of
these vessels.

The lymphatic drainage from the different parts of the colon bears a direct
relationship to arterial blood supply.

Ulcerative Colitis.

Ulcerative colitis is an inflammatory disorder that affects the rectum and extends
proximally to affect a variable extent of the colon. The cause of the disease and the
factors determining its chronic course are unknown.

The disease was first recognized as an entity distinct from bacillary dysentery by
Samuel Wilks, a physician at Guy's Hospital in 1859.

Ulcerative colitis is a worldwide disorder, although its precise incidence varies.

High-incidence areas include the United Kingdom, the United States, Northern Europe,
and Australia. Among whites, the incidence ranges from 3 to 15 cases per 100,000
persons per year, with a prevalence of 80 to 120 per 100,000. Low-incidence areas
include Asia, Japan, and South America. It is difficult to obtain accurate figures but the
 incidence rates are probably about 10-fold less in low-incidence areas than in high-
incidence areas.

Ulcerative colitis primarily affects young adults (20 to 40 years of age). Women
tend to be affected more commonly than men.

In the United States, Jews are more prone to ulcerative colitis than are non-Jews.
In Baltimore, the incidence among Jews was 13 per 100,000 persons compared with 3.8
per 100,000 among non-Jewish whites.

Etiology. The cause is unknown. No organisms or group of organisms can be

incriminated.

Possibly the disease is linked with emotional stress.

It may be related to genetic abnormalities disease.

Some cases are allergic to milk protein. In cases of extensive ulceration

secondary infection plays a large part.

In some families there is a strong tendency for the disease to occur in successive
generations: either a genetic predisposition is inherent in the members of these families,
or an unidentified environmental factor is present.

Pathology. Approximately 20% of patients have total colitis, 30% to 40% have
disease extending beyond the sigmoid but not involving the whole colon, and 40% to
50% have disease limited to the rectum and rectosigmoid. In 95% of cases the disease
starts in the rectum and spreads proximally. When the ileocaecal valve is incompetent,
retrograde ileitis involving the last foot (30cm) of the ileum is liable to occur.

The disease is characterized by the appearance of multiple minute ulcers; in

some cases the ulcers are discrete. Microscopical nearly always proves that the
ulceration is more severe and extensive with many small abscesses ("crypt abscess")
beneath the mucosa.

When the ulceration extends into the submucosa it may cause reflex muscle
spasm and the appearance of stricture. In longstanding cases there is always
considerable intramural fibrosis, causing the affected part of the colon to become
permanently contracted. Strips of oedematous mucosa may be elevated between
ulcerated areas ("pseudopolyposis"). With time, persistent recurrent attacks of
inflammation can lead to mucosal atrophy or disorientation; if these latter changes
become severe, precancerous changes can develop (severe dysplasia, carcinoma in
situ).

Clinical Features. The onset of the disease is more in women than in men in the
3rd, 4th, and 2nd decade.

The major symptoms of ulcerative colitis include diarrhea, rectal bleeding, the
passage of mucus, and abdominal pain. The symptom complex tends to differ according
to the extent of disease, but generally the severity of the symptoms correlates with the
severity of the disease.

The first symptom is watery diarrhea occurring day and night. A rectal discharge
of mucus, sometimes blood-stained and sometimes purulent is very common.
Symptoms have usually been present for weeks, or even months, by the time a patient
presents to a physician; the slow, insidious onset is characteristic of the disease.

Patients with a hemorrhagic proctitis (i.e., inflammation confined to the rectum)

usually complain of passing fresh blood, either separately from the stool or streaked on
the surface of a normal or hard stool. When the disease extends beyond the rectum,
blood is usually mixed with stool or there may be grossly bloody diarrhea. However,
most patients with active disease complain of diarrhea—the frequent passage of loose or
liquid stool—and may have nocturnal diarrhea. Postprandial diarrhea is common. For
most patients with ulcerative colitis, pain is not a prominent symptom. Some patients
with active disease may experience vague lower abdominal discomfort, an ache in the
left iliac fossa, or mild central abdominal cramping. Severe cramping and abdominal
pain can occur in association with severe attacks of the disease. Patients with mild or
even moderately severe disease exhibit few abnormal physical signs. They are usually
well nourished and not anemic and show no signs of chronic disease.

Disease of moderate or severe activity may often be associated with systemic

symptoms. Patients may become anorectic and nauseated and, in severe attacks, may
vomit. These symptoms, as well as protein loss through inflamed mucosa,
hypercatabolism, account for weight loss and hypoalbuminemia, which may be
profound. Fever, an additional catabolic factor, usually accompanies severe attacks.
Patients also may complain of the symptoms of anemia, such as breathlessness, ankle
swelling, and fatigue. The anemia is secondary to blood loss, but may drug-induced
causes (6-mercaptopurine, azathioprine, sulfasalazine).

The severity of disease can be ascertained by various criteria, as follows. A

guide to disease severity:
  Mild. Fewer than four stools daily, with or without blood, with no
systemic disturbance and a normal erythrocyte sedimentation rate (ESR).

 Moderate. More than four stools daily but with minimal systemic
disturbance.

 Severe. More than six stools daily with blood and with evidence of
systemic disturbance, as shown by fever, tachycardia, anemia, or an ESR greater
than 30.

In the majority of cases, the disease is chronic, characterized by relapses and

remissions.

In general a bad prognosis is indicated by:

a- A severe initial attack

b- Disease involving the whole colon

c- Increasing age; especially after 60 years.

Clasifications. Several kinds of disease are encountered:

1- Limited colitis. The disease remains confined to rectum and distal colon. The
risk of cancer is very low in such cases. 5-10% of cases spread to involve the rest of the
colon.

2- Total colitis is the form for which the title ulcerative colitis should be used.
This form has maximal risks for complications and after 10 years of disease life there is
a greatly enhanced risk of cancer which raises to 10 tomes the normal population after
15 years.

The clinical pattern is one of recurrent severe attacks, with bloody diarrhea (up to
20 times daily), dehydration and fluid and electrolyte losses during attacks. Anemia and
hypoproteinaemia are common. Total colectomy is frequently resorted to for these
cases.

3- Fulminating type is ushered in with temperature of 38.9-39.4 and incessant

diarrhea containing blood, mucus, and pus. The patient looks and feels very ill. There
may be abdominal distention due to toxic dilatation of the colon, which can be confirmed
by plain abdominal X-ray. Here immediate surgery is indicated. The term fulminant is
used to describe a particularly severe attack, but this term is best avoided because its
meaning is ambiguous.

The condition must be differentiated from dysentery, typhoid, and amoebic colitis.
 A low serum albumin level is associated with the degree of severity of an attack
and can influence the decision to operate.

4- Chronic type. As a rule the initial attack is of moderate severity, but the
disease settles into a persistent low-grade illness. The frequency of the motions and the
degree of invalidism go hand in hand, and are proportional to the extent of the
involvement of colon. Lesions of limited length are commonly found in milder cases.

Sigmoidoscopy is indispensable in the diagnosis of early cases and in mild

cases when the pathological effects of disease are insufficient to alter the barium
shadow. The initial findings are those of proctitis: the mucosa is hyperemic, bleeds on
touch and there is considerable exudate. Later, tiny ulcers may be seen. As the disease
progresses, the ulceration may become so severe that practically no normal mucous
membrane remains. Sigmoidoscopic assessment is useful for describing the
macroscopic appearance of the colonic mucosa. A convenient grading system is as
follows:

 0—Normal mucosa

 1—Loss of vascular pattern

 2—Granular, nonfriable mucosa

 3—Friability on rubbing

 4—Spontaneous bleeding, ulceration.

Rectal biopsy is essential not only in establishing the diagnosis, but also as an
index of the effect of therapy and progress of the disease.

A barium enema should be avoided during the fulminating phase.

Radiology after a barium enema shows one of the following:

- The earliest sign is loss of haustration, especially in the distal colon.

- In many cases, an instant enema (water soluble contrast without bowel

preparation) will show mucosal changes (ulceration especially involving lengths of the
rectum and colon).

- Alterations of the mucosal pattern such as pseudopolyposis.

32.30 Ulcerative colitis. Loss of haustial markings in the descending colon

( inflammation and ulceration of the mucosal lining) in contrast with their
presence in the transverse colon.
 32-33 -Mucosal pseudopolyp formation in the desending colon

- In chronic cases, a narrow contracted (pipe-stem) colon may be demonstrated.

Colonic Complications:

1- Pseudopolyposis -15%

2- Carcinoma: the overall risk is about 3.5%. After 20 years of the disease the
risk may be as much as 12%. Carcinomatous change often atypical and high-grade may
occur at many sites at once.

3- Fibrous stricture occurs in 6% of cases. The common sites are the

rectosigmoid junction and the anal canal. Simple dilatation. Surgery if the whole colon is
involved.

4- Toxic dilatation occurs in the fulminating type of the disease. It may result in
perforation. Both require immediate surgery. Frequently the only sign that the
perforation has occurred is the abdominal distention. This is cardinal sign of impeding
doom without immediate intervention.

5- Massive hemorrhage.

6- Rectovaginal fistulas and fistula in ano.

7- Ischiorectal abscess (4%) and hemorrhoids (20%) also occur.

8- Ectopic complications. Liver changes such as cirrhosis occur 4%

9- Skin lesions -18.5%. Pyoderma gangrenosum (0.5%) and erythema

nodosum (2%).

10- Arthritis, iritis (7%), ankylosing spondylitis (2%), stomatitis (10%), renal
disease (5%), anemia (20%), sclerosing cholangitis (1%), carcinoma of the bile
duct (1%).

Treatment.

The main general principles are:

1- Maintenance of the fluid and electrolyte balance.

2- Anemia must be rapidly corrected.

3- Adequate nutrition- at least 3000 Cal/day- with high protein, carbohydrates,

and vitamin content and low fat.

4- Sedatives and tranquilizers are useful. Antibiotics may precipitate moniliasis.

 Specific treatment:

- Quiescent cases are best maintained on sulphasalazine (2g/day).

Mild to moderate relapses the dose of sulphasalazine is increased (4-6g/day).

- Topical steroid.

- Retention enemas of prednisolone phosphate 20mg in 100ml daily.

Acute fulminating cases. Systemic prednisolone 20mg or more daily may be

required for up to 3 weeks.

Indications for surgery:

1- To save life- fulminating cases, toxic dilatation, severe hemorrhage,

perforation.

2- Colonic complications.

3- Ectopic complications.

4- Risk of neoplastic change.

5- Onset in children or adolescents.

6- Chronic invalidism.

When surgical treatment (15-20%) is advised, about 6 days intensive

preoperative preparation by the methods already enumerated is carried out.

Operations.

1- The classical procedure is a one-stage total proctocolectomy with

ileostomy.

2- Total colectomy + iliorectal anastomosis. If the ileorectal anasromosis

unsound + a temporary loop ileostomy proximal to the anstomosis is employed.

22-55 Subtotal colectomy as performed for ulcerative colitis as for diffuse

polyposis of the colon.

22.57 Ileorectal anastomosis following subtotal colectomy.

3- Ileostomy alone: for a gravely ill patient with fulminating disease and
localized abscess around a perforation. A paste of aluminium (10 parts and zinc oxide
90 parts) is helpful. A paste of karaya gum.

32-32 -An end –ileostoma.

 4- Total proctocolectomy and ileoanal pouch: this operation substitutes a
pouch of ileum for the rectum and allows for normal defecation if successful (special
coloproctological institutes).

32-35 -End- to-end ileoanal anastomosis following colectomy,

mucosal proctectommy and endorectal ileoanal pull-through.

32.36 Ileal pouch configurations in patients undergoing endorectal

ileoanal anastomosis.

68.26 Ileoanal anastomosis with pouch:

a) a simple reversed “j”,

b) a “S”pouch,

c) a “W” pouch.

68-27 Stapled “j” pouh with stapler creating a pouch – anal anastomosis.

Diverticular Disease of the Colon.

Diverticula of the colon are acquired herniations of colonic mucosa protruding

through the circular muscle at the points where the blood vessels penetrate the colonic
wall. Thus they tend to occur in rows in between the strip of longitudinal muscle (taenia
coli). Diverticular disease of the colon includes a constellation of symptoms that range
from mild irregularities in defecatory function to severe bleeding and the consequences
of severe intra-abdominal inflammation.

32 – 7 Transverse section of the colon demonstrating the relationship of

diverticula to colonic taenia and vasculature.

The earliest pathologic description of chronic diverticula is traditionally attributed

to Cruveilhier in 1849. The presence of uncomplicated pseudodiverticula, herniations of
the mucosa and submucosa through the muscular coat of the colon, was defined
asdiverticulosis from radiographic studies by Case in 1914.
 The true prevalence of diverticular disease is not known. In the United States and
other developed countries, the prevalence approaches 10%.

Common to many acquired abnormalities, age is an important variable.

Diverticulosis is uncommon before age 40 and increases in frequency with age. Autopsy
reports suggest that it is found in up to one half of adults above the age of 60.

The condition most often is localized to one part of the colon, usually the sigmoid.
In 90% of cases the sigmoid colon is involved and becomes almost always the site of
inflammation i.e. diverticulitis.

32.8 Diagram illustrating the prevalence of diverticular disease by

location within the colon.

Diverticular disease is rare in Africans and Asiatics who eat a diet which
contains natural fibers. In Western countries, diverticula are found in 5% of barium
enemas over the age of 40, and the incidence increases with age.

Diverticulosis. The pathogenesis of diverticular disease is multifactorial,

as the population and pathologic studies suggest. The anatomic features intrinsic
to the colon, alterations in colonic wall with aging, motor dysfunction, abnormal
increases in intraluminal pressure, and dietary fiber may all contribute to the
development of diverticulosis in ill-defined interrelationships.

Most diverticula in the colon are actually pseudodiverticula, consisting of

herniations of the mucosa and submucosa through the muscular coat of the colon.
Although true diverticula, containing all layers of the bowel wall, do occur as
congenital anomalies, the more common pulsion pseudodiverticula are acquired .
The points of greatest muscular weakness are where the intramural vasa recta
penetrate the circular muscle to the submucosa.

The interplay of hypersegmentation resulting in intraluminal hypertension

and the low-bulk Western diet have implicated as the primary cause of diverticular
disease. Intraluminal manometry has shown that intracolonic pressures may
exceed 90 mm Hg when segmentation allows the motor work of the colonic
musculature to be transmitted to the bowel wall rather than producing transit of
feces.

Fiber increases stool weight, lowers colonic pressures, and improves transit
time.
 Clinical Features. Most diverticulosis patients have no symptoms or such
minor symptoms that they never seek medical attention. Some patients have
symptoms such as intermittent abdominal pain, bloating, excessive
flatulence, and irregular defecation. Nausea, anorexia, passage of pellet-like
stools, or attacks of diarrhea may also be present. Rectal bleeding is uncommon
in uncomplicated diverticular disease.

The primary stage of the disease is called painful diverticular disease and is
related to muscular incoordination and spasm resulting in increased segmentation and
intralumenal pressure. This may lead to diverticulum formation.

Most patients suffer from long standing constipation.

Emotion and drugs like morphine and prostigmine increase segmentation and
intracolonic pressure.

Differential diagnosis. Many conditions, especially those associated with

altered intestinal motility, may be confused with diverticular disease. The most common
of these is irritable bowel syndrome, although the most important entity to consider is
carcinoma.

Treatment. Diverticulosis should be treated with a high residue diet containing

roughage in the form of whole meal bread and flour, fruit and vegetables. Bulk formers
such as bran may be given until the stools are soft. The ingestion of 20 to 30 g of bran
is necessary to achieve a therapeutic effect.

Diverticulitis is the secondary stage. Diverticulitis results from inflammation of

a colonic diverticulum with subsequent perforation. Diverticulitis is the most common
complication of diverticulosis, occurring in 10% to 25% of patients. The initial event is a
microperforation of the bowel through a diverticulum, which results in a
peridiverticulitis and/or phlegmon and is referred to as uncomplicated diverticulitis .

Clinical Features of diverticulitis:

- Persistent lower abdominal pain in the left iliac fossa.

- Fever, malaise.

- Loose stools or may be constipated.

- Abdominal distention.

The lower abdomen is tender especially on the left. The sigmoid colon may be
palpable, tender, and thickened.
 Leukocytosis help to differentiate diverticulitis from painful diverticular disease.

The condition is essentially progressive: the longer the duration, the worse are
the symptoms and the grater the risk of complications.

The third stage is complicated diverticulitis. Complicated diverticulitis ensues if

continuation of the inflammatory and septic process is associated with obstruction,
free perforation, fistula, or abscess. With repeated episodes the phlegmonous
reaction becomes more extensive, and with healing, the fibrotic reaction may ensheathe
the colon and produce segmental narrowing, stricture, or even obstruction.

The complications are:

1- Recurrent periodic inflammation and pain.

2- Perforation leading to general peritonitis or

3- Local (pericolic) abscess formation.

4- Intestinal obstruction due to progressive fibrosis causing stenosis.

5- Hemorrhage.

6- Fistula formation. The septic process may erode into adjacent structures and
produce a fistula. The most common is the colovesical fistula. Other common fistulas
are colocutaneous, colovaginal, and coloenteric fistulas. Fistula formation occurs in
about 5% of cases.

Diverticulitis is not a precancerous condition, but cancer may coexist.

Colonoscopy has proved to be useful in differentiating diverticular disease from
carcinoma.

Diagnosis. The diagnosis of acute diverticulitis is made on clinical grounds and

is confirmed by barium enema and sigmoidoscopy only when any acute inflammation
has subsided as an enema given in an acute attack may cause perforation and
peritonitis.

Radiology. Barium enema may show diverticula and the typical narrowed
sigmoid .

-"Saw tooth" appearance of the "prediverticular state". Such spastic strictures are
sometimes relaxed by pro-Banthine and this may help to differentiate them from
neoplasm.
 32.13 Barium enema demonstrating a typical case of severe diverticulosis.
Pancolonic disease.

32.14 Barium enema demonstrating a severe stricture in the sigmoid colon

secondary to diverticula disease.

Sigmoidoscopy may be painful. The mucosa inflamed. The bowel may be rigid,
narrow, and acutely angled at about 15 cm so that the instrument cannot be passed
further.

Treatment of Uncomplicated Diverticulitis .

Severity of the inflammatory and infectious process determines the treatment for
diverticulitis. Patients can be treated on an outpatient basis if they have minimal
symptoms or signs of inflammation. A clear liquid diet is recommended, and broad-
spectrum antibiotics such as metronidazole plus ciprofloxacin are continued for 7 to 10
days.

Signs of significant inflammation indicate that the patient should be hospitalized

for bowel rest, intravenous fluids, and broad-spectrum intravenous antibiotics, such as
ampicillin sodium/sulbactam sodium (Unasyn); metronidazole plus a cephalosporin
(such as cefotetan) or less commonly an aminoglycoside such as gentamicin. If pain,
medication is required, parenteral meperidine hydrochloride is an appropriate analgesic
as it has been shown to decrease intraluminal pressure.

Morphine and enemas are contraindicated.

4- Fistulas. Diverticular fistula results from diverticulitis with an associated

abscess that erodes into an adjacent organ. A tract is established between the source of
the abscess (perforated sigmoid diverticulum) and the secondarily involved adjacent
organ. This is a relatively frequent complication of diverticulitis and has been reported in
5% to 33% of diverticular disease patients requiring an operation.

A large variety of fistulas have been described in diverticular disease patients.

Colovesical fistula is the most common variety, followed by colocutaneous, colovaginal,
and coloenteric fistulas.

Patients who have a colovesical fistula often have symptoms of urinary tract
infection (75%) and pneumaturia (60%).

Barium enemas have been reported to demonstrate the communication in only

50% of cases but confirm the presence of diverticular disease.
 Cystograms have been shown to demonstrate the fistula in approximately 30%
of cases.

Cystoscopy demonstrates the internal opening in less than 50% of patients,

although some abnormality has been demonstrated in 90% of patients.

The general principle of treating fistulas is to remove the offending organ of

origin. After the diseased bowel is resected, a primary anastomosis is constructed.

Postoperative urinary drainage usually using a Foley catheter should be

continued for at least 7 days. A cystogram may be performed prior to removing the
Foley catheter to ensure that there is no leakage from the bladder.

5- Hemorrhage. Painless rectal bleeding is associated with diverticulosis in 15%

to 40% of patients.

Although this bleeding is usually of minor clinical significance, massive bleeding

from colonic diverticula may occur in 5% of patients who have diverticulosis, often
requiring blood transfusion.

The cause appears to be chronic injury to the vasa recta adjacent to the lumen of
the diverticulum.

Emergency angiography has become the initial procedure of choice for

patients who experience brisk bleeding. The superior mesenteric artery is studied first,
as the incidence of acute bleeding is highest from the right side. Next, the inferior
mesenteric artery is studied, to be followed by the celiac axis injection, which may show
an unsuspected upper intestinal bleeding site.

Nuclear scanning techniques using technetium 99m sulfur colloid (99mTcSC)

and technetium-tagged red blood cells may be useful for patients who experience a
slower rate of bleeding.

In most patients who have diverticular hemorrhage, the bleeding stops

spontaneously.

Supportive medical care, including volume resuscitation and component therapy

of coagulation abnormalities, stabilizes the condition of those patients who have a low
transfusion requirement. The subset of patients who have hypotension or an ongoing
transfusion requirement need prompt intervention, as these frequently elderly patients
have significant morbidity and mortality rates.
 Emergency surgery is clearly indicated in the treatment of persistent or recurrent
diverticular bleeding. The most important factor in both safety and efficacy of emergency
surgery is a clear definition of the bleeding site during preoperative investigations.

Embolization of the affected vessel with autologous blood or absorbable

gelatin powder (Gelfoam) is also effective. However, postembolic colonic infarction is
a significant risk.

Appropriate segmental colectomy yields a very low rebleeding rate. Most

surgeons have concluded that subtotal colectomy remains the procedure of choice in
this subset of patients.

Operative Procedures for Diverticular Disease.

About 10% of the patients require operation, either for recurrent attacks which
make life a misery or for complication.

1- The ideal operation done as an interval procedure after careful preparation of

the gut is a one-stage resection. Resection and primary anastomosis is the most
common operation employed for patients who can have bowel preparation prior to
surgery. This is a one-stage procedure in which the diseased segment of bowel is
removed and intestinal continuity is restored. For patients who have recurrent
uncomplicated diverticulitis, this procedure is the standard operation performed.

Laparoscopic colorectal surgery has been performed since 1991, but

acceptance and application by surgeons have been slow. One reason is that
laparoscopic colorectal surgery is significantly more difficult than most other advanced
laparoscopic procedures. Recently, there has been increasing interest among surgeons
to learn and implement laparoscopic colectomy in their practice.

Laparoscopically assisted anterior resection for diverticular disease has

been demonstrated to have acceptable morbidity and mortality rates with a shorter
hospital stay and improved cosmetic and functional results. Several series have
documented that laparoscopic surgical techniques for diverticular disease are safe,
although challenging, with a conversion rate to a standard open laparotomy from
laparoscopic technique of less than 10%. Even in cases of complicated diverticular
disease with fistula, laparoscopically assisted colectomy has been shown to be an
effective means of treatment.

Another major concern has been the increased cost because of longer operating
times and the significant cost associated with operating room charges. Although
operating room charges were higher in laparoscopic patients, the total hospital charges
and costs were markedly lower in one series.

2- If there is inflammation, a preliminary transverse colostomy can be done as a

first stage. The second stage: resection is performed after 3 weeks or later when the
inflammation has subsided. The colostomy is closed after a further 2 weeks (third
stage).

3- Free perforation from diverticulitis into the peritoneal cavity results in

generalized peritonitis. Intra-abdominal findings are classified as purulent peritonitis or
the more devastating form of feculent peritonitis.

Purulent peritonitis may arise from the sudden rupture of a previously walled-off
pericolic or pelvic abscess or from a persistently leaking diverticular perforation. .
Prompt resuscitation and preoperative preparation are begun. The mortality rate for
feculent peritonitis patients has been reported at 35%-50% compared with 6%-15% for
those with diffuse purulent peritonitis.

There is a choice of procedures:

a) Proximal colostomy with suture of perforation.

b) Exteriorization of the affected bowel which is then opened as a colostomy.

Transverse colostomy and drainage, as the first step of a three-stage

procedure, was the traditional recommendation for patients with perforated sigmoid
diverticulitis and abscess formation. This procedure should only be performed when
peritonitis and the inflammatory process are so severe that resection of the perforated
segment cannot be safely accomplished.

c) Resection with Sigmoid Colostomy and Closure of the Rectal Stump

(Hartmann's Procedure).

Hartmann's procedure was named for Henri Hartmann, the French surgeon who
described it as the treatment for proximal rectal cancer in 1923. This procedure has
become the most common operation for the emergency treatment of diverticulitis. The
advantage of this two-stage procedure is that the septic focus is removed by the primary
operation and the source of continued contamination is eliminated.

After resection the peritoneal cavity should be copiously irrigated with warm
saline solution. All the above procedures must be accompanied by drainage of the
abdomen. Single drainage alone should be reserved for a localized pericolic abscess.
 Crohn's Disease (Regional Enteritis).

Crohn's disease is a condition of chronic inflammation potentially involving

Hystory. Although the eponymous "Crohn's disease" has gained general

acceptance in recent years, clear clinicopathologic reports of the same process
date back at least two centuries.
any location of the alimentary tract from mouth to anus but with a propensity for the
distal small bowel and proximal large bowel.

The landmark publication of Crohn, Ginzburg, and Oppenheimer in 1932 called

attention to "terminal ileitis" as a distinct and chronic entity.

The term "regional enteritis" embraced the focal nature of the process.

The term "granulomatous enterocolitis" lost acceptance when it became clear

that granulomas were not a sine qua non of the diagnosis.

Epidemology. Age-adjusted annual incidence rates of 6.0 and 10.0 cases per
100,000 persons have been reported. In Japan, the incidence rate has remained low,
with estimates between 0.08 and 0.5 per 100,000. Crohn's disease is thought to be
extremely rare in much of South America and Africa.

Most reports show a female-to-male ratio 1.2:1.

Etiology. Crohn's disease represents a state of sustained immune response.

Many infectious agents have been proposed as the causative organism of

Crohn's disease. No causative organism has been found. Among the most enduring
hypotheses is that Mycobacterium paratuberculosis is the causative agent of Crohn's
disease.

Poor barrier function may be a factor in the onset of Crohn's disease.

Abnormally increased intestinal permeability is also found, suggesting a possible
genetic susceptibility.

The argument for a genetic predisposition in Crohn's disease begins with the
observation that family members of affected persons are at greatly increased risk of
developing Crohn's disease. The relative risk among first-degree relatives is 14 to 15
times higher than that of the general population.

Crohn's has been associated with higher socioeconomic status.

 Fruits and vegetables in the diet have been associated with the development of
Crohn's disease by exacerbation of symptoms in patients with mild disease by
increased dietary fiber intake.
Many studies have discerned an increased risk of Crohn's disease among
women who use oral contraceptives.

Crohn's disease is more prevalent among smokers, and smokers have more
surgery for their disease and a greater risk of relapse after resection.

Pathology. Focal intestinal inflammation is the hallmark pathologic finding in

Crohn's disease. This tendency for focal inflammation is evident in focal crypt
inflammation, focal areas of marked chronic inflammation, the presence of aphthae and
ulcers. The earliest lesion characteristic of Crohn's disease is the aphthous ulcer .
These superficial ulcers are minute, ranging in size from barely visible to 3 mm, and are
surrounded by a halo of erythema.

It usually commences at or near the ileocaecal valve and extends upwards along
the ileum for about 30cm.

Contact with luminal contents is a key factor in the development of aphthous

ulcers in Crohn's disease. Aphthous ulcers heal in bowel excluded from the fecal stream
by ileostomy.

The presence of granulomas are highly characteristic of Crohn's disease.

The classic cobblestone appearance may arise, representing a network of

ulcers surrounding relatively normal mucosa and prominent submucosal edema. Ulcers
may extend to the muscularis propria.

31.14 Photograph of ileum, cecum and ascending colon resected

for Crohn”s disease of the terminal ileum, which demonstrates ulcerated ileal
mucosa with a cobblestone appearance thickened bowel wall and
enlarged adjacent ileal lymph nodes.

The presence of lymphoid aggregates in both the submucosa and external to

the muscularis propria are an accurate sign of Crohn's disease even when granulomas
are not seen.

Large ulcers, sinus tracts, and strictures are late features of Crohn's
disease.
 31-17 Radiograph of terminal ileum, cecum and ascending colon involved
by Crohn’s disease, demonstrating mucosal ulceration with a cobblestone
appearance, thickened bowel wall and luminal narrowing.

With penetration of inflammation to the serosa, serositis may occur, resulting in

adhesion of bowel to other loops of large or small bowel or other adjacent organs. As a
result of the chronicity of the inflammatory process, free perforation is much less
common than walled-off or contained intra-abdominal abscesses or fistulas to bowel,
skin, bladder, or vagina.

Fibrosis is another transmural aspect of the disease. Fibrosis may be evident

grossly as irregular thickening of the bowel wall and, may contribute to the development
of stricture.

31-19 Radiograph of large intestine with Crahn’s disease. Note the areas
of narrowing with mucosal ulceration in the transverse colon, descending colon
and sigmoid colon, with spared dilated segments of healthy colon and rectum in
between.

At the anatomic level, one of the most characteristic findings of Crohn's disease
is the presence of fat wrapping . This finding, virtually pathognomonic of Crohn's
disease, is the encroachment of mesenteric fat onto the serosal surface of the bowel.

In acute cases the affected intestine is seen to be swollen, bright pink in color,
and with a fibrinous exudate on its peritoneal surface. The mesentery of the involved
intestine is exceedingly thickened, edematous, and contains enlarged and fleshy lymph
nodes. Above the diseased ileum upwards there is commonly another short area of
diseased intestine. This is a so-called skip lesion.

In chronic cases on palpation the intestinal wall feels like a hose-pipe.

Examples of primary Crohn's disease of the colon, jejunum, duodenum, and even
of the stomach and anus has been reported, which justifies the newer term, regional
enteritis. Crohn's colitis is now nearly as common as the ileal form in some series.

Clinical Features.

The disease is independent of age, sex, social, and economic conditions, or

geographical location. To some extent it is familial.
 The presentation of Crohn's disease may be subtle and varies considerably.
Factors contributing to this variability include the location of disease within the
gastrointestinal tract, intensity of inflammation, and presence of specific intestinal and
extraintestinal complications.

Abdominal pain may be intermittent and colicky in nature or sustained and

severe. Some patients may experience symptoms that are mild but long-standing or that
are atypical. Such patients are more likely to experience a delay in diagnosis in excess
of 1 year.

Fecal occult blood may be found in roughly one half of patients, but gross rectal
bleeding is uncommon, and acute hemorrhage is rare.

Constitutional symptoms, particularly weight loss and fever, or growth

retardation in children may also be prominent and are occasionally the sole presenting
features of Crohn's disease.

Chronic Crohn's disease is the usual form of the disease.

First stage. Mild diarrhea. Intestinal colic. Intermittent pyrexia. A tender mass
can be felt in the right iliac fossa. Moderate secondary anemia. Occult blood, and some
mucous are present in the stools. A perianal abscess is a frequent accompaniment of
early Crohn's disease. The cause is probably an infected anal crypt associated with the
concomitant diarrhea.

Second stage. Characterized by symptoms of acute or chronic intestinal

obstruction.

Third stage. Adhesions form: adhesions are dense.

Abscess formation is common, and fistulous tracts tend to develop which can be:

- Internally: enterocolic and vesicointestinal fistulas.

- Externally: nearly always through the scar of a previous operation for the
condition e.g. appendicectomy.

Disease of the ileum

Disease of the ileum, often accompanied by involvement of the cecum, may

present insidiously. Some patients may present initially with a small bowel
obstruction, perhaps precipitated by impaction of indigestible foods such as raw
vegetables or fruit. Many years of subclinical inflammation may progress to fibrotic
stenosis, with the subsequent onset of intermittent colicky pain, sometimes
accompanied by nausea and vomiting. Physical examination may reveal fullness
or a tender mass in the right hypogastrium during obstructive episodes. Patients
with an active inflammatory component to their disease more often present with
anorexia, loose or frequent stools, and weight loss. Examination may reveal fever
or evidence of malnutrition. Occasionally, a patient may present with a more acute
onset of right lower quadrant pain, mimicking appendicitis.

Colonic disease may involve primarily the right colon or may extend distally to
involve most or the entire colon ( extensive or total colitis ). The typical presenting
symptom is diarrhea, occasionally with passage of obvious blood.

The severity of inflammation and the presentation may range from minimally

Fistulas are frequent manifestations of the transmural nature of Crohn's disease.

Perianal fistulas are common, estimated to occur among 15% to 35% of patients.

Fistulas from one segment of the gastrointestinal tract to another also occur
frequently. Enteroenteric, enterocolonic, and colocolonic fistulas are often
asymptomatic.

Fistula to the vagina may occur with penetration from a severely inflamed rectal
vault anteriorly as a rectovaginal fistula or from the small bowel ( Enterovaginal
fistula).

Enterovesicular or colovesicular fistulas may present as recurrent

polymicrobial urinary tract infection or as frank pneumaturia and fecaluria.

Enterocutaneous fistulas to the anterior abdomen, often occurring after

surgery. A classic presentation of Crohn's disease is the onset of an enterocutaneous
fistula after appendectomy for what had been presumed to be appendicitis.
altered bowel habits to fulminant colitis. Systemic manifestations such as weight loss
and malaise may also be prominent

Many as one fourth of all patients with Crohn's disease will present with an intra-
abdominal abscess at some time in their lives.
 Stricture is another characteristic complication of Crohn's disease. Strictures
represent long-standing inflammation and may occur in any segment of the
gastrointestinal tract in which inflammation has been active. Symptoms may
include colicky postprandial abdominal pain and bloating, punctuated by more
severe episodes, and often culminating in complete obstruction.
The classic radiographic "string sign" of a markedly narrowed bowel segment in
a widely spaced bowel loop is a result of spasm and edema associated with active
inflammation rather than fibrostenosis. All strictures must be considered with suspicion,
and biopsies of a stricture need to be pursued vigorously because some strictures will
harbor cancer.

Radiological diagnosis.

Complications are the same as for ulcerative colitis, except that the cancer risk is
very low and is maximal in the ileum.

Acute Crohn's disease occurs only in 5% of cases. The symptoms and signs
resemble those of acute appendicitis with one exception which is diarrhea almost
invariably precedes the acute attack.

Exceptionally, perforation of the intestine resulting in local or diffuse peritonitis

Differential Diagnosis.
occurs. Acute colitis with toxic megacolon can occur with Crohn's disease but is rarer
than in ulcerative colitis.

There are a number of clinical situations in which Crohn's disease should enter
the differential diagnosis: functional bowel disorders, primarily irritable bowel syndrome;
immune-mediated diseases, and most importantly ulcerative colitis, drug-related
causes, especially NSAIDs; vascular causes, notably ischemic bowel disease and
collagen vascular diseases; neoplasia, including carcinoma and lymphoma; infectious
causes of diarrhea, gut inflammation, or granulomas and other diseases and
syndromes, including diverticular disease.

Differentiating Crohn’s Disease from Ulcerative Colitis. Discriminating

features include small bowel disease, predominantly right colonic disease, rectal
sparing, fistulization, major perianal complications, and granulomas, all of which are
strongly indicative of Crohn's disease.

Treatment.

- Bed rest.

- High protein diet with vitamin supplementation.

 - Iron or blood transfusions may be required.

Medical Therapy.

Aminosalicylates. Aminosalicylates are often used in the treatment of mild to

moderate Crohn's disease. Sulfasalazine, the parent compound of all aminosalicylates
used in IBD. -

- Antibiotics: gentamycin, metronidazole, sulphaphthalidine, salazopirin or

steroids: prednisone, prednisolone. ACTH depot.

In the acute form of the disease - azathioprine,

- Nasogastric or parenteral feeding.

Indications for surgery:

1- Failure to arrest the course of the disease by adequate medical treatment.

2- Intestinal obstruction.

3- Presence of fistulas.

Operations:

1- Right hemicolectomy.

31.21 -Diagram of resection of the ileum, ileocolonic valve, cecum and

ascending colon for Crohn’s disease of the ileum. Intestinal continuity is restored by
end-to-end ileal ascending colostomy.

2- Segmental resection.

3- Colectomy and ileorectal anastomosis.

4- Temporary ileostomy.

5- Stricture plasty.

31-22 Diagram of “stricturoplasty “for localized segment of Crohn’s

disease of the small bowel.A longitudinal incision. A subsequent transverse
closure with sutures.

6- Panproctocolectomy and permanent ileostomy.