Small bowel

Alaa maali
INTESTINAL OBSTRUCTION

INFECTIVE ENTERITIS

TUMOURS OF THE SMALL INTESTINE

CONNECTIVE TISSUE DISORDERS ) diverticulae)

VASCULAR ANOMALIES OF THE INTESTINE .


CONDITIONS CAUSING MALABSORPTION
Intestinal obstruction : two types:
Dynamic :
●● Intraluminal : Faecal impaction , Foreign bodies,
Bezoars, Gallstones.
 ●● Intramural : Stricture , Malignancy ,
Intussusception ,Volvulus .
●● Extramural: Bands/adhesions, Hernia.

Adynamic :
●● Paralytic ileus ●● Pseudo-obstruction
PATHOPHYSIOLOGY
the bowel proximal to the obstruction dilates and the
bowel below the obstruction exhibits nor mal
peristalsis and absorption until it becomes empty and
collapses.

Initially, proximal peristalsis is increased in an attempt

to overcome the obstruction. If the obstruction is not
relieved, the bowel continues to dilate; ultimately there
is a reduction in peristaltic strength, resulting in
flaccidity and paralysis.
The distension proximal to an obstruction is caused by
two factors:
Gas: overgrowth of both aerobic and anaerobic
organisms, resulting in considerable gas production
(following the reabsorption of oxygen and carbon dioxide,
the majority is made up of nitrogen (90%) and hydrogen
sulphide).

Fluid: made up of the various digestive juices. (saliva

500 mL, bile 500 mL, pancreatic secretions 500 mL,
gastric secretions 1 litre – all per 24 hours). This
accumulates in the gut lumen as absorption by the
obstucted gut is retarded.
STRANGULATION : the blood supply is compromised
and the bowel becomes ischaemic.

Causes of strangulation :
 Direct pressure on the bowel wall : Hernial orifices ,
Adhesions/bands

Interrupted mesenteric blood flow : Volvulus ,

Intussusception

Increased intraluminal pressure : Closed-loop obstruction

Distension of the obstructed segment of bowel results
in high pressure within the bowel wall. Venous return
is compromised before the arterial supply. The
resultant increase in capillary pressure leads to
impaired local perfusion and once the arterial supply is
impaired, haemorrhagic infarction occurs.
Closed-loop obstruction
the bowel is obstructed at both the proximal and distal
points The distension is principally confined to the
closed loop
 SPECIAL TYPES OF MECHANICAL
INTESTINAL OBSTRUCTION
**Internal hernia : a portion of the small intestine becomes
entrapped in one of the retroperitoneal fossa or in a congenital
mesenteric defect.
The following are potential sites of internal herniation (all are
rare):
● the foramen of Winslow.
● a defect in the mesentery.
● a defect in the transverse mesocolon.
● defects in the broad ligament
● congenital or acquired diaphragmatic hernia.
● duodenal retroperitoneal fossa.
● appendiceal retroperitoneal fossa
**Obstruction from enteric strictures :
secondary to tuberculosis or Crohn’s disease.
Malignant strictures associated with lymphoma are
uncommon.
 whereas carcinoma and sarcoma are rare.
 Presentation is usually subacute or chronic.
**Bolus obstruction :
Gallstones : tends to occur in the elderly secondary to
erosion of a large gallstone directly through the gall
bladder into the duodenum.
Food : may occur after partial or total gastrectomy when
unchewed articles can pass directly into the small bowel.
Trychobezoars and phytobezoars : firm masses of
undigested hair ball and fruit/ vegetable fibre respectively.
phytobezoars : high fibre intake, inadequate chewing,
previous gastric surgery, hypochlorhydria and loss of the
gastric pump mechanism.
Stercoliths: usually in association with a jejunal diverticulum
or ileal stricture.
Worms : Ascaris lumbricoides
 Obstruction by adhesions and bands
Adhesions: In Western countries adhesions and bands are the
most common cause of intestinal obstruction.
 The lifetime risk of requiring an admission to hospital for
adhesional small bowel obstruction susequent to abdominal
surgery is around 4% and the risk of requiring a laparotomy
around 2%.
 Adhesions start to form within hours of abdominal surgery.

 Prevention of adhesions : Good surgical technique ,Washing

of the peritoneal cavity with saline to remove clots ,
Minimising contact with gauze , Covering anastomosis and raw
peritoneal surfaces.
 Acute intussusception
one portion of the gut invaginates into an immediately
adjacent segment; almost it is the proximal into the distal.
most commonly in children, with a peak incidence
between 5 and 10 months of age.
About 90% of cases are idiopathic but an associated upper
respiratory tract infection or gastroenteritis may precede
the condition.(hyperplasia of Peyer’s patches )
An intussusception is composed of three parts :
● the entering or inner tube (intussusceptum)
 ● the returning or middle tube
 ● the sheath or outer tube (intussuscipiens).
 Volvulus
twisting or axial rotation of a portion of bowel about its
mesentery.
>180° torsion ... Obstruction
>360° torsion... vascular occlusion in the mesentery
may be primary (congenital malrotation) or
secondary(acquired adhesion or stoma) .
The commonest spontaneous type in adults is sigmoid
CLINICAL FEATURES OF INTESTINAL
OBSTRUCTION

influenced by whether the obstruction is:

small bowel obstruction (high or low) / large bowel
obstruction.
Complete/ incomplete.
simple / strangulating.
Location , the underlying pathology;
Pain : is the first symptom encountered; sudden ,severe,
colicky in nature and usually centred on the umbilicus.
the colicky pain is replaced by a mild and more constant
diffuse pain. If there is no ischaemia and the obstruction
persists over several days, pain reduces and can
disappear.

Vomiting : The more distal the obstruction, the longer

the interval between the onset of nausea and vomiting.
 As obstruction progresses the character of the vomitus
alters from digested food to faeculent material, as a result
of the presence of enteric bacterial overgrowth.
Distension : the degree of distension is dependent on the
site of the obstruction and is greater the more distal the
lesion.

Constipation : This may be classified as absolute (neither

faeces nor flatus is passed) or relative (where only flatus is
passed). Absolute constipation is a cardinal feature of
complete intestinal obstruction.
Some patients may pass flatus or faeces after the onset of
obstruction as a result of the evacuation of the distal bowel
contents.
Other manifestations :
A) Dehydration (repeated vomiting and fluid
sequestration)
B) Hypokalaemia : not a common
C) Pyrexia : rare and may indicate: ischaemia ,
perforation, inflammation or abscess.
D) Abdominal tenderness .
E) Bowel sounds : High-pitched , may absent if the
obstruction is longstanding and the small bowel has
become inactive.

Clinical features of strangulation :

Constant pain, severe pain , Tenderness with rigidity and
peritonism , Shock.
DIAGNOSIS :
History and Physical exam.
Confirm by abdominal series: Supine abdominal x-ray ,
Upright abdominal x-ray , Upright chest radiograph .
Abdominal computed tomographic (CT)
TREATMENT : If the patient is stable or has partial
SBO, give a trial of nonoperative management:
 NPO.
 IV hydration to counter effects of third spacing.
Nasogastric tube (NGT) for gastric decompression;
decreases nausea, vomiting, distention.
 Foley catheter to monitor urine output.
Monitor electrolytes for signs of hypokalemia, base defi
cit/metabolic acidosis (signs of ischemia)

**Patients with suspected strangulation need to be

resuscitated with fl uids prior to surgery.
If the patient fails conservative management (24 hrs
without improvement, abdominal tenderness worsens,
fever, other signs of clinical deterioration), then
laparotomy should be performed.

The surgical procedure depends on the cause of the

obstruction : A) Adhesions call for lysis of adhesions
(LOA).
B) Hernias should be reduced and repaired or, if contents
of sac are strangulated, needs intestinal resection.
C) Cancer requires en bloc resection with lymph node
sampling.
D) Crohn’s disease requires resection or stricturoplasty of
affected area only.
Whatever the cause, the entire small bowel should be
examined, and nonviable intestine should be resected.
INFECTIVE ENTERITIS :
1) Campylobacteriosis

 2) Yersiniosis

3) Salmonellosis

4) Tuberculosis

5) Actinomycosis
1) Campylobacteriosis
Infection with Campylobacter jejuni (a gram-negative
rod with a distinctive spiral shape) .
 the most common form of bacterial gastroenteritis in the
UK.
 typically acquired from eating infected poultry.
 It causes diarrhoea and abdominal pain and may mimic
an acute abdomen. Severe cases may resemble UC, with
rectal bleeding and colorectal ulceration, causing
diagnostic difficulty.
 Treatment is generally supportive as the condition
usually resolves without antibiotics.
2) Yersiniosis
Yersinia enterocolitica is a gram-negative rod that can infect
the terminal ileum, appendix, ascending colon and
mesenteric lymph nodes.

can cause a granulomatous inflammatory process that mimics

CD. typically causes a fever and gastroenteritis, but may
persist and cause a terminal ileitis, which may perforate.

Diagnosis : stool culture , confirmed serologically.

 normally self-limiting, but responds to treatment with
cotrimoxazole or chloramphenicol .
3) Salmonellosis, typhoid and
paratyphoid.
Salmonella are a family of gram-negative rods .
Salmonella gastroenteritis is typically caused by S.
enteritidis from poultry, and is most often a self-
limiting illness comprising headache, fever and watery
diarrhoea.

diagnosis is based on stool culture.

 Shigella and enteropathogenic strains of E. coli may

cause similar diarrhoeal illnesses.
Typhoid fever is caused by S. typhi and presents with fever
and abdominal pain after an incubation period of 10–20
days.

Over the next week, the patient can develop distension,

diarrhoea, splenomegaly and characteristic ‘rose spots’ on
the abdomen caused by a vasculitis.

Typhoid is a systemic infection , invasion of the systemic

circulation, which is a characteristic feature of
salmonellosis, may cause severe gram-negative sepsis,
resulting in septic shock. Some patients develop metastatic
sepsis, including septic arthritis and osteomyelitis,
meningitis, encephalitis, disseminated intravascular
coagulation and pancreatitis.
Perforation of a typhoid ulcer characteristically occurs
during
the third week of the illness. The ulcer is parallel to the long
axis of the gut and is usually situated in the distal ileum.

Perforation requires surgery to wash out and close the ulcer

 diagnosis : culture of blood or stool.
 Treatment: antibiotics (chloramphenicol).

Paratyphoid infection (with S. paratyphi) resembles typhoid

fever and is treated in a similar manner.
 4) Tuberculosis of the intestine
can affect any part of the gastrointestinal tract from the
mouth to the anus , most often ileum, proximal colon
and peritoneum.

- There are two principal disease presentations:

A) Ulcerative tuberculosis
B) Hyperplastic tuberculosis
 A) Ulcerative tuberculosis
 develops secondary to pulmonary tuberculosis and arises as a
result of swallowing tubercle bacilli.
** Multiple ulcers, lying transversely, develop in the terminal
ileum and the overlying serosa is thickened, reddened and covered
in tubercles. -- Patients typically present with diarrhoea and weight
loss, obstruction ,perforation and fistula formation can occur.
 A barium follow-through or CT examination fails to show filling
of the lower ileum, caecum and the ascending colon as a result of
narrowing of the ulcerated segment .
Treatment : A course of antituberculous chemotherapy usually
leads to cure, provided the pulmonary tuberculosis is adequately
treated. Surgery is usually undertaken only in the rare event of a
perforation or complete intestinal obstruction.
 B) Hyperplastic tuberculosis
caused by the ingestion of Mycobacterium tuberculosis by patients with
a high resistance to the organism.

 usually occurs in the ileocaecal region, (solitary and multiple ).

** chronic inflammation causes thickening of the intestinal wall and

narrowing of the lumen. There is early involvement of the regional
lymph nodes, abscess and fistula formation are rare . There is
incomplete ileal obstruction, leading to stasis and bacterial overgrowth.
This in turn causes steatorrhoea, anaemia and loss of weight.
abdominal pain and diarrhoea.
** Patients may present with a mass in the right iliac fossa and vague ill
health.(D.D appendix mass, lymphoma, carcinoma of the caecum, CD,
tuberculosis or actinomycosis.)
 diagnosis : barium follow-through ,small bowel enema ,
CT (narrowed segment with proximal distension and the
associated lymphadenopathy)

Treatment : ** When the diagnosis is clear and the

patient has not yet developed obstructive symptoms,
chemotherapy is advised and may be curative.
**Where obstruction is present, or the possibility of CD
or lymphoma require clarification, ileocaecal resection is
often required.
 5) Actinomycosis
 infection with Actinomyces israelii , usually develops
several weeks after an apparently straightforward
perforated appendicitis
Develop abscess and fistulation .
** mesenteric lymph nodes are not involved and the
lumen of the intestine is not narrowed.
 Haematogenous spread via the portal vein may lead to
multiple liver abscesses.

Treatment : Penicillin or cotrimoxazole (prolonged and in

high dosage) .
 Human immunodeficiency virus (HIV)
Intestinal complications are common after the
development of AIDS when opportunistic organisms can
cause gastroenteritis .

Opportunistic intestinal infections in patients with

AIDS:
 ●● Bacteria: Salmonella ,Shigella ,Yersinia,
Campylobacter , Mycobacterium avium intracellulare
(MAI) .
●● Viral : Cytomegalovirus .
●● Protozoa: Cryptosporidium, Giardia
 ●● Fungal: Candida albicans
 TUMOURS OF THE SMALL
INTESTINE
rare and in total account for less than 10% of gastrointestinal
neoplasia.
 Benign : The majority of small bowel neoplasms
are benign, comprising adenomas, lipomas, haemangiomas
and neurogenic tumours.
frequently asymptomatic and identified incidentally, but can
present with intussusception, obstruction and
bleeding( anaemia , overt )
Symptomatic lesions can be treated by small bowel resection
and anastomosis.
Peutz–Jeghers syndrome
autosomal dominant disease characterised by melanosis
of the mouth and lips, with multiple hamartomatous
(benign tumour-like) polyps in the small bowel and colon.
The gene STK11 on chromosome 19 has been found in a
proportion of patients with this condition.
Reduce survival as a consequence of complications of
bowel obstruction and the development of a range of
cancers.
 Despite the increased risk of malignancy in general,
malignant change in the polyps themselves rarely occurs
and polyps can be left alone unless they are the cause of
symptoms.
Resection may be indicated, however, for heavy and

persistent or recurrent bleeding or intussusception.

Polyps may be removed by enterotomy or, at
laparotomy, snared via a colonoscope introduced via an
enterotomy. Heavily involved segments of small
intestine may occasionally be resected.
 Malignant :
Small bowel malignancy is rare and classically presents
late, most often diagnosed after surgery for small bowel
obstruction.

 Four types will be considered, which account for over

99% of small bowel malignancies: adenocarcinoma,
carcinoid tumours, lymphomas and mesenchymal
tumours (gastrointestinal stromal tumours [GIST]).
 Adenocarcinoma
Mostly in jejunum.
 more common in patients with CD, coeliac disease,
familial adenomatous polyposis, hereditary non-polyposis
colon cancer and Peutz–Jeghers syndrome.
present with anaemia, overt gastrointestinal bleeding,
intussusception or obstruction.
Prognosis is poor .
When suspected, the advised surgical treatment is a
resection of 5 cm of non-involved bowel either side of the
lesion and the affected mesentery , right hemicolectomy is
likely to be required for tumours of the distal ileum.
 Carcinoid tumours
neuroendocrine tumours occur throughout the
gastrointestinal tract, most commonly in the appendix,
ileum and rectum.
arises from Kulchitsky cells at the base of intestinal crypts.
In up to one-third of cases of small bowel carcinoids, the
tumours are multiple.
can produce a number of vasoactive peptides, most
commonly serotonin, but also histamine, prostaglandins .
When they metastasise to the liver, the ‘carcinoid
syndrome’ can become evident, because the vasoactive
substances escape the filtering actions of the liver.
Carcinoid syndrome:
 ●● Diarrhoea
 ●● Bronchospasm
●● Facial/upper chest flushing
●● Palpitations
●● Tricuspid regurgitation
Dignosis : The extent of disease can be assessed preoperatively
using octreotide scanning, which may detect otherwise clinically
unapparent primary and secondary tumours.

Plasma markers of tumour , such as chromogranin A may be

useful markers of disease recurrence, as well as of prognostic
value.

Treatment : Surgical resection is usually sufficient for patients

with primary disease, but the incidence of recurrence is
significant. octreotide (a somatostatin analogue)

Hepatic resection can be carried out in patients with metastatic

disease.
They are not usually sensitive to chemo- or radiotherapy.
Carcinoid tumours generally grow more slowly than
most metastatic malignancies and patients may live
with the syndrome of metastatic disease for many
years.
Lymphoma
Small bowel lymphoma may be primary or, more
commonly, secondary to systemic lymphoma.
The incidence is increased in patients with CD and
immunodeficiency syndromes.
 most western-type lymphomas are non-Hodgkin’s B-cell
lymphomas. They usually present with anaemia,
bleeding, perforation, anorexia and weight loss.
T-cell lymphoma develops in patients with coeliac disease.
It usually presents with worsening of the patient’s
diarrhoea, pyrexia of unknown origin and local
obstructive symptoms.
Burkitt’s lymphoma can aggressively affect the ileocaecal
region, particularly in children.
The mainstay of Treatment for these conditions is
chemotherapy; however, surgery may be required for
obstruction, perforation or bleeding.
 Gastrointestinal stromal tumours
 mesenchymal tumours and the distinction between benign
or malignant types is difficult even on histological
examination.

 Increased size and high levels of c-kit (CD117) staining

are associated with malignant potential.
 found most commonly in the stomach, but can be found
in other parts of the gut.
They occur most commonly in the 50- to 70-year age
group.
patients with neurofibromatosis have an increased risk of
developing these types of tumour.
Patients may be asymptomatic and the tumour may
present as an incidental mass on a CT scan.
Symptoms include lethargy, pain, nausea, haematemesis
or melaena.

Treatment : Surgery , Glivec® (imatinib) is a tyrosine

kinase inhibitor that has been shown to be effective in
advanced cases and may also have a role in adjuvant
treatment.
CONNECTIVE TISSUE
DISORDERS
) Intestinal diverticulae (
Diverticulae (hollow out-pouchings) are a common
structural abnormality that can occur from the
oesophagus to the rectosigmoid junction .

 may be congenital or acquired

 Acquired diverticulae
 develop in the jejunum and arise from the mesenteric side
of the bowel as a result of mucosal herniation at the point
of entry of the blood vessels ( no muscularis layer in the
wall).
can vary in size and are frequently multiple.
They are commonly asymptomatic and present as an
incidental finding at surgery or on radiological imaging.
However, they can result in malabsorption, as a result of
bacterial stasis, or present as an acute abdominal
emergency if they become inflamed or perforate.
 Bleeding from a jejunal diverticulum is a rare
complication (compared with sigmoid diverticular disease)
 If perforated jejunal diverticulitis is found at emergency
laparotomy, a small bowel resection should be performed
and a decision made between anastomosis and stoma
formation. This will depend on the degree of
contamination, physiological stability and local resources
for managing a patient with a high output jejunostomy.

In severe cases, much of the proximal small intestine may

be involved, effectively precluding resection. Prolonged
antibiotic therapy for bacterial overgrowth may be
preferable
Meckel’s diverticulum
congenital true diverticulum .

Remnant of the omphalomesenteric duct (vitelline) , which

connects the yolk sac with the primitive midgut in the
embryo.

 It may be vulnerable to obstruction and inflammation in

the same way as the appendix ; indeed, when a normal
appendix is found at surgery for suspected appendicitis, a
Meckel’s diverticulum should be looked for by examining
the small bowel, particularly if free fluid or pus is found.
” rule of 2s ” :

Found in 2% of the population

2% of patients are asymptomatic .

Found 2 feet (60 cm ) from the ileocecal valve

Mostly are 2 inches (5 cm) long

Most symptoms occur before age 2 year

Ectopic tissue found in 1 of 2 patients (gastric, colonic or pancreatic

type)

2 to 1 male : female ratio

present clinically in the following ways:

 ● Haemorrhage, painless dark rectal bleeding or melaena.

 ● Diverticulitis, presents like appendicitis, if perforation
occurs the presentation may resemble a perforated duodenal
ulcer.
● Intussusception, ileoileal or ileocolic intussusception.
 ● Chronic ulceration, Pain is felt around the umbilicus
 ● Intestinal obstruction , A band between the apex of the
diverticulum and the umbilicus may cause obstruction directly,
or by predisposing to the development of a volvulus around it.
 ● Perforation.
The finding of a Meckel’s diverticulum in an inguinal or
femoral hernia has been described as ‘Littre’s hernia’.
 VASCULAR ANOMALIES OF THE
INTESTINE .
Mesenteric ischaemia : Mesenteric vascular disease may
be classified as acute intestinal ischaemia – with or
without occlusion –, chronic , central or peripheral.
The superior mesenteric vessels are the visceral vessels
most likely to be affected by embolisation or thrombosis.
 Occlusion at the origin of the SMA is almost the result
of thrombosis.
emboli tend to lodge at the origin of the middle colic
artery.
Inferior mesenteric involvement is usually clinically
silent because the collateral circulation is better.
Possible sources for embolisation of the SMA include:
 the left atrium in atrial fibrillation
 the left ventricle after mural myocardial infarction.
 vegetations on mitral and aortic valves associated with
endocarditis and an atheromatous plaque from an aortic
aneurysm.
 Primary thrombosis is associated with atherosclerosis and
vasculitides, including conditions such as thromboangitis
obliterans and polyarteritis nodosa.
Primary thrombosis of the superior mesenteric veins may
occur in association with : factor V Leiden, portal
hypertension, portal pyaemia ,and sickle cell disease and
in women taking the oral contraceptive pill.
Irrespective of whether the occlusion is arterial or venous,
haemorrhagic infarction occurs. The mucosa is especially
sensitive to ischaemic injury because of its high metabolic
activity. The intestine and its mesentery become swollen
and oedematous, especially with venous occlusion.

The changes develop rapidly and irreversible injury,

ranging in severity from mucosal necrosis and sloughing,
to full- thickness infarction usually occurs within a few
hours at most.

Clinical features : The most important clue to an early
diagnosis of acute mesenteric ischaemia is the sudden
onset of severe abdominal pain in a patient with atrial
fibrillation or atherosclerosis. The pain is typically in the
central abdomend . Persistent vomiting and defaecation
occur early, with the subsequent passage of altered blood.
Abdominal tenderness may be mild initially, with rigidity
being a late feature. Shock, with features of both
hypovolaemia and sepsis, rapidly ensues.
Investigation will usually reveal a profound neutrophil
leucocytosis with an absence of gas in the lumen of the
thickened small intestine on abdominal radiographs and
CT scans. Gas may be present within the intestinal wall
and occasionally in the mesenteric and portal veins.
Treatment : In conjunction with full resuscitation,
laparotomy with embolectomy via the ileocolic artery or
revascularisation of the SMA by vascular bypass may be
considered in early cases. Anticoagulation should be
implemented early in the postoperative period.

However, the condition is usually diagnosed late in the

disease process and the mortality rate is extremely high.
In the young, all affected bowel should be resected,
whereas in the elderly or infirm the situation may be
deemed incurable.
 Chronic small intestinal ischaemia

almost results from atherosclerosis and affects the proximal

superior mesenteric and coeliac vessels.
Patients classically present with symptoms of severe central
abdominal pain that comes on within 30–60 minutes of
eating (mesenteric angina). Weight loss and diarrhoea due
to malabsorption may also occur.

Treatment : is usually by selective visceral angiography,

with stenting/angioplasty and, where this is not possible,
bypass surgery.
CONDITIONS CAUSING MALABSORPTION
Celiac disease : the most common cause of malabsorption
in the UK with a stated prevalence of 1:1800.
It is characterised by a hypertrophic small bowel mucosa
with atrophic villi and deep crypts.
 loss of surface area and brush border enzymes results in
malabsorption.
 caused by an abnormal immune response to gluten , There
is a genetic component, as the disease is more common in
first-degree relatives and has an association with HLA B8.
In children, coeliac disease presents with steatorrhoea
and growth retardation.

In adults, it may result in diarrhoea and weight loss

but many patients simply present with an iron
deficiency anaemia. Some patients develop a
characteristic skin rash (dermatitis herpetiformis)
Diagnosis : usually made after an endoscopic duodenal
biopsy allows pathological examination of mucosa
(flattening of the mucosa, marked inflammatory changes
and characteristic findings of intraepithelial lymphocytes).

 The antiendomysial antibody tests have a very high

sensitivity and specificity for coeliac disease, but a
duodenal biopsy is usually indicated to confirm the
diagnosis.

Patients with coeliac disease may develop an acute

inflammatory condition of the small intestine and have an
increased risk of small bowel lymphoma and
adenocarcinoma.
The main treatment for coeliac disease is the
withdrawal of gluten from the diet by avoiding wheat,
rye and barley. Surgery does not usually play a role in
the management of coeliac disease and is primarily
reserved for resection of malignancy.
 Bacterial overgrowth
The small intestine can become colonised with bacteria
normally confined to the colon if there is stasis resulting in
delayed bacterial clearance (blind loop syndrome).
Similar complications may result from chronic small
bowel obstruction, jejunal diverticulosis and ileosigmoid
fistulation.
If overgrowth occurs in the upper small intestine, the
defect is chiefly of fat absorption; if in the lower intestine,
there is vitamin B12 deficiency.
Sometimes, the only manifestation is anaemia, resulting
from vitamin B12 deficiency but, if steatorrhoea occurs,
other serious malabsorption features may follow, including
glossitis, osteomalacia, paraesthesia and peripheral
Treatment :
Improvement normally follows after intermittent
therapy with oral antibiotics; metronidazole,
ciprofloxacin, tetracycline and rifaximin are commonly
used.
Definitive treatment is surgical when the anatomical
abnormality can be corrected, but this is not always
possible.
 SHORT BOWEL SYNDROME
Intractable diarrhoea with impaired absorption of nutrients
following resection or bypass of the small intestine leading
to progressive malnutrition .
The most common causes :
resection resulting from the management of CD (50%)
mesenteric vascular thrombosis.
 radiation enteritis
Tumours

Although features of short bowel syndrome usually appear

when there is less than 200 cm of small bowel, the length
and nature of the remaining intestine are also important
there is some evidence that the ileum, with its tighter
intercellular junctions and consequently better fluid
absorptive capacity, can assume the functions of a missing
jejunum, but not vice versa.

Patients with an intact colon are relatively protected from

the effects of massive small bowel resection because of the
ability of the colon to absorb not only fluid and
electrolytes, but a modest amount of nutrient energy.
Patients with as little as 100–200 cm of jejunum
anastomosed to an intact colon may therefore be able to
maintain satisfactory macronutrient, fluid and electrolyte
status, although they will, of course, be at risk of fat-
soluble and B12 vitamin deficiencies and will also
generally need oral nutritional supplements of trace
Some patients with 50–100 cm of small intestine and an
intact colon will need long-term parenteral nutrition, as
will almost all patients with 50 cm or less of jejunum
anastomosed to an intact colon.
In contrast, most patients with less than 200 cm of small
intestine ending in a jejunostomy will require regular
infusions of parenteral fluid and electrolytes, and almost
all of those with less than 100 cm of small bowel ending
in a jejunostomy will require long-term parenteral
nutrition.
Medical management of patients with short bowel
syndrome relies on the use of antidiarrhoeal agents
(loperamide and codeine phosphate), drugs to reduce
diarrhoea related to bile-salt malabsorption (colestyramine)
and enteral and parenteral vitamin and trace element
supplements , drugs to promote intestinal adaptation such
as growth hormone, glutamine and, most recently,
glucagon-like peptide 2 agonists.

the mainstay of treatment is home parenteral nutrition

(HPN). The development of this treatment in the late 1960s
enabled the majority of patients with short bowel
syndrome to enjoy a reasonably good quality of life, with
long-term survival related principally to the underlying
disease
HPN is, however, expensive and demanding and patients with
short bowel syndrome receiving HPN are at risk from
catheter-related complications (notably catheter-related
sepsis and occlusion), as well as metabolic complications
(fibrotic liver disease, gallstones, metabolic bone disease and
kidney stones).

Surgical : improve the surface area or reduce the speed of

transit of the remaining small intestine have shown some
promise in children.
complications of long-term intravenous feeding or the
development of progressive liver dysfunction may represent
indications for small bowel transplantation. The results of
small bowel transplantation have progressively improved and
5-year patient survival now exceeds 80% in some centres.