all about small intestine, anatomy, physiology, intestinal obstruction, crohns disease/ileostomy/viscous organ perforation, meckels diverticulum, mysenteric ischemia, short bowel syndrome, celiac disease

1. SMALL INTESTINE
Dr Rajeev Kumar Pandit
FCPS 1st Yr Surgery Resident
Manmohan Memorial Medical College
Swoyambhu, Nepal

2. GROSS ANATOMY
• Extends from the pylorus to the cecum.
• Measure 4 to 6 m.
• Three segments lying in series:
• the duodenum,
• the jejunum, and
• the ileum
• Internal mucosal folds known as plicae circulares or valvulae conniventes
• Most of the duodenum derives its arterial blood from branches of both
the celiac and the superior mesenteric arteries.
• The distal duodenum, the jejunum, and the ileum derive their arterial
blood from the superior mesenteric artery.

3. • Their venous drainage occurs via the superior mesenteric vein.
• Lymph drainage occurs through lymphatic vessels coursing parallel to
corresponding arteries.
• This lymph drains through mesenteric lymph nodes to the cisterna chyli,
then through the thoracic duct, and ultimately into the left subclavian
vein.
• The parasympathetic and sympathetic innervation of the small intestine is
derived from the vagus and splanchnic nerves, respectively.

5. • Small intestine consists of four distinct layers: mucosa, submucosa,
muscularis propria, and serosa

6. DEVELOPMENT
• Formed from the endoderm during the fourth week of gestation.
• The gut tube is divided into forgut, midgut, and hindgut.
• Other than duodenum, which is a forgut structure, the rest of the
small intestine is derived from the midgut.
• The gut tube initially communicates with the yolk sac; however, the
communication between these two structures narrows by the sixth
week to form the vitelline duct.
• The yolk sac and vitelline duct usually undergo obliteration by the end
of gestation

7. • Incomplete obliteration of the vitelline duct results in the spectrum of
defects associated with Meckel’s diverticulum
• The portion of mesoderm that adheres to the endoderm forms the
visceral peritoneum, while the portion that adheres to the ectoderm
forms the parietal peritoneum.
• This mesodermal division results in the formation of a coelomic cavity
that is the precursor of the peritoneal cavity.

9. PHYSIOLOGY
• Digestion and Absorption
• The intestinal epithelium is the interface through which absorption and
secretion occur.
• Solutes can traverse the epithelium by active or passive transport.
• Passive transport of solutes occurs through diffusion or convection and is driven
by existing electrochemical gradients.
• Active transport is the energy-dependent net transfer of solutes in the absence
of or against an electrochemical gradient.
• Active transport occurs through transcellular pathways (through the cell),
whereas
• Passive transport can occur through either transcellular or paracellular pathways
(between cells through the tight junctions)

17. SMALL BOWEL OBSTRUCTION

21. Clinical Presentation
• Abdominal distention
• Most pronounced if the site of obstruction is in the distal ileum and may be absent
if the site of obstruction is in the proximal small intestine
• Colicky abdominal pain
• Nausea
• Vomiting
• Vomiting is a more prominent symptom with proximal obstructions than distal
• The vomitus is more feculent, suggesting a more established obstruction
• Obstipation
• Continued passage of flatus and/or stool beyond 6 to 12 hours after onset of
symptoms is characteristic of partial rather than complete obstruction

22. • Physical examination
• Tachycardia
• Hypotension
• Fever suggests the possibility of strangulation
• Distended abdomen
• Severe dehydration signs
• Mild abdominal tenderness
• Localized tenderness, rebound, and guarding suggest peritonitis and the likelihood
of strangulation
• In early stage - hyperactive bowel sounds with audible rushes associated with
vigorous peristalsis (borborygmi).
• In Late minimal or no bowel sounds
• Rectal examination should always be performed to assess for intraluminal masses
and to examine the stool for occult blood.

23. Radiologic and Laboratory Studies
• Plain Abdominal X ray
• Supine - dilated loops of small intestine, without evidence of colonic distention.
• Upright - demonstrate multiple air-fluid levels, which often layer in a stepwise pattern
• The finding most specific for small bowel obstruction is the triad of dilated small bowel
loops (>3 cm in diameter), air-fluid levels seen on upright films, and a paucity of air in the
colon
• Also demonstrate the cause of the obstruction
• USG and CT scan
• Strangulation is suggested by thickening of the bowel wall, pneumatosis intestinalis (air in
the bowel wall), portal venous gas, mesenteric haziness, and poor uptake of intravenous
contrast into the wall of the affected bowel
• Lab findings
• Serum sodium, chloride, potassium, bicarbonate, and creatinine levels
• Serial determination of serum electrolyte levels
• Leukocytosis

24. Treatment
• Conservative therapy
• Fluid Resuscitation and Antibiotics
• NG decompression
• Commonly recommended in the initial treatment for:
1. Partial small bowel obstruction
2. Obstruction occurring in the early postoperative period
3. Intestinal obstruction due to Crohn’s disease
4. Carcinomatosis
Nonoperative management has been documented to be successful in 65% to
81% of patients with partial small bowel obstruction
5% to 15% have been reported to have symptoms that were not substantially
improved within 48 hours after initiation of therapy

26. Operative Management
• Performed for small bowel obstruction varies according to the
etiology of the obstruction. For example, adhesions are lysed, tumors
are resected.
• Depends upon the cause of obstruction.
• Laparoscopic surgery

27. Outcomes
• Prognosis is related to the etiology of obstruction
• Mortality rates associated with surgery for strangulating obstruction
range from 8% to 25%.

28. Prevention
• Strategies for adhesion prevention
• Good surgical technique
• Careful handling of tissue
• Minimal use and exposure of peritoneum to foreign bodies form the
cornerstone of adhesion prevention
• Use of hyaluronan based agents, such as Seprafilm

29. Internal herniation
• Occurs when a portion of the small intestine becomes entrapped in one
of the retroperitoneal fossae 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 fossae – left paraduodenal and right duodenojejunal;
• Caecal/appendiceal retroperitoneal fossae – superior, inferior and retrocaecal;
• Intersigmoid fossa.

30. Gallstone ileus
• Occur in the elderly
• Secondary to erosion of a large gallstone directly through the gall bladder into
the duodenum.
• Classically, there is impaction about 60 cm proximal to the ileocaecal valve
• Recurrent attacks ---- ball-valve effect
• Radiological sign of gallstone ileus is Rigler’s triad
• Small bowel obstruction,
• Pneumobilia and
• Atypical mineral shadow on radiographs of the abdomen.
• At laparotomy, the stone is milked proximally away from the site of impaction.
• It may be possible to crush the stone within the bowel lumen; if not, the
intestine is opened at this point and the gallstone removed

31. Bands
• Usually only one band is culpable.
• This may be:
• Congenital, e.g. obliterated vitellointestinal duct;
• A string band following previous bacterial peritonitis;
• A portion of greater omentum, usually adherent to the parietes.

32. Acute intussusception
• One portion of the gut invaginates into an immediately adjacent segment.
• 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.
• Hyperplasia of Peyer’s patches in the terminal ileum may be the initiating
event.
• Weaning, loss of passively acquired maternal immunity and common viral
pathogens have all been implicated in the pathogenesis of intussusception in
infancy

33. • In children -- Meckel’s diverticulum, polyp, duplication, Henoch–Schönlein
purpura or appendix
• Pathology
• An intussusception is composed of three parts
• the entering or inner tube (intussusceptum);
• the returning or middle tube;
• the sheath or outer tube (intussuscipiens).

34. Clinical Presentation
• In pediatric group
• Shortly after the onset of pain, vomiting may occur.
• Nearly half of cases progress to stool mixed with blood and mucus, giving it a
“currant jelly” appearance.
• Physical exam may reveal a palpable “sausage-shaped mass” in the right
upper quadrant or epigastric region of the abdomen, but the mass is only
detected in approximately 60% of cases
• Adult
• Classic triad of abdominal pain, palpable mass, and bloody stool

35. • Ultrasonography
• The classic feature is the target or doughnut sign caused by the edematous
intussuscipiens forming an external ring around the centrally based intussusceptum.
• On the transverse view, the pseudo-kidney appearance is formed by the layers of
the intussusception.
• In adults, however, ultrasound tends to be less accurate than in children, but may
still reveal classic features of the target or doughnut sign on the transverse view and
pseudo-kidney on the longitudinal view.
• CT scan is the investigation of choice, where a “target sign” may be seen.

37. • Treatment is surgical resection of the involved segment and the lead
point, which needs to undergo pathologic evaluation to rule out an
underlying malignancy.
• Reduction by ultrasound-guided or fluoroscopic pneumatic or
hydrostatic enema, and is successful in 85 to 90% of cases.
• Close observation is required due to the heightened possibility of
recurrence within the first 24 hours.
• Retrograde intussusception;- proximal bowel is drawn in to the
lumen of the distal bowel.

38. Volvulus
• A volvulus is a twisting or axial rotation of a portion of bowel about its
mesentery.
• The rotation causes obstruction to the lumen (>180° torsion) and if tight
enough also causes vascular occlusion in the mesentery (>360° torsion).
• Bacterial fermentation adds to the distension and increasing intraluminal
pressure impairs capillary perfusion.
• Mesenteric veins become obstructed as a result of the mechanical twisting
and thrombosis results and contributes to the ischaemia.
• Volvuli may be primary or secondary.
• The primary form occurs secondary to congenital malrotation of the gut,
abnormal mesenteric attachments or congenital bands. Examples include
volvulus neonatorum, caecal volvulus and sigmoid volvulus.
• A secondary volvulus, which is the more common variety, is due to rotation
of a segment of bowel around an acquired adhesion or stoma.

39. Presentation can be classified as:
Fulminant: sudden onset, severe pain, early vomiting, rapidly
deteriorating clinical course
Indolent: insidious onset, slow progressive course, less pain, late
vomiting.

40. Returning of motility after laparotomy
• Small-intestinal motility returning to normal within the first 24 hours
• Gastric by 48 hours
• Colonic motility by 3 to 5 days
• Functional evidence of coordinated GI motility in the form of passing
flatus or a bowel movement is a more useful indicator

41. ILEUS

43. CROHN’S DISEASE
• Chronic, idiopathic transmural inflammatory disease with a propensity to
affect the distal ileum, although any part of the alimentary tract can be
involved
• Females > Males
• Third decade of life years & sixth decade of life
• Genetic and environmental factors influence
• Approximately one in five patients with Crohn’s disease will report having
at least one affected relative
• Higher socioeconomic status --- increased risk of Crohn’s disease
• Smoking is associated with the increased risk of need of surgery and
relapse.

44. Pathophysiology
• Inflammation response to a yet unrecognized pathogen or an inappropriate response
to a normally innocuous stimulus is unknown.
• As disease progresses, aphthae coalesce into larger, stellate-shaped ulcers.
• Linear or serpiginous ulcers may form when multiple ulcers fuse in a direction parallel
to the longitudinal axis of the intestine.
• With transverse coalescence of ulcers, a cobblestoned appearance of the mucosa may
arise.
• Transmural inflammation.
• Serosal involvement results in adhesion
• Can also result in fibrosis with stricture formation,
• Intra-abdominal abscesses,
• Fistulas and
• Free perforation.
• Inflammation in Crohn’s disease can affect discontinuous portions of intestine—so-
called “skip lesions” that are separated by intervening normal-appearing intestine
• Presence of fat wrapping

45. Clinical Presentation
• Abdominal pain (right lower quadrant), diarrhea, and weight loss
• Depend on
• Which segment(s) of the GI tract is (are) predominantly affected the
• Intensity of inflammation, and
• The presence or absence of specific complications
• Classified by their predominant clinical manifestation as having
primarily
(a) Fibrostenotic disease,
(b) Fistulizing disease,
(c) Aggressive inflammatory disease

46. • Extraintestinal
manifestation in one
fourth of cases

47. Diagnosis
• Usually established with endoscopic findings in a patient with a compatible
clinical history.
• Colonoscopy with intubation of terminal ileum
• Focal ulcerations
• Polypoid mucosal changes that give a “cobblestone appearance.”
• Skip lesions
• Strictures on contrast study
• CT scan - may reveal intra-abdominal abscesses
• Esophagogastroduodenoscopy (EGD) for proximal bowel involvement.
• Antibody tests
• ASCA +/pANCA– Crohn’s disease
• ASCA–/pANCA+ Ulcerative colitis
• Vitamin B12 deficiency

48. D/D
• Ulcerative colitis,
• Acute appendicitis
• Irritable bowel syndrome,
• Mesenteric ischemia,
• Collagen vascular diseases,
• Carcinoma and lymphoma,
• Diverticular disease, and
• Infectious enteritides
• Mycobacterium tuberculosis
• Salmonella typhosa
• Cytomegalovirus (CMV)

50. Therapy
• No curative therapies are available for Crohn’s disease, the goal of
treatment is to palliate symptoms rather than to achieve cure.
• Medical therapy is used to induce and maintain disease remission.
• antibiotics, aminosalicylates, corticosteroids, and immunomodulators
• Surgery is reserved for specific indications

51. • Oral 5-aminosalicylic acid (5-ASA) drugs (e.g., mesalamine)
• First line of treatment
• Oral glucocorticoids
• Used to treat patients with mildly to moderately severe disease that does not respond
to aminosalicylates.
• Patients with severe active disease usually require intravenous administration of
glucocorticoids.
• Should be tapered once remission is achieved
• Steroid dependence and steroid resistant---- use of immune modulators should be
considered
• Thiopurine antimetabolites azathioprine and its active metabolite, 6-
mercaptopurine,
• Have demonstrated efficacy in inducing remission, in maintaining remission, and
• In allowing for glucocorticoid tapering in glucocorticoid-dependent patients.
• A response to these medications is usually observed in 3 to 6 months

52. • Anti–tumor necrosis factor-α (TNF-α) antibody—infliximab
• Generally used for patients resistant to standard therapy, in order to help taper steroid
dosage
• Surgical Therapy
• Failure of medical management
• Intestinal obstruction
• Abscesses and fistulas

53. INTESTINAL FISTULAS

54. • A fistula is defined as an abnormal communication between two
epithelialized surfaces.
• Internal fistula --- communication between two parts of the GI tract or
adjacent organs(e.g., enterocolonic fistula or colovesicular fistula).
• External fistula --- involves the skin or another external surface
epithelium(e.g., enterocutaneous fistula or rectovaginal fistula).
• Low-output fistulas ----- drain less than 200 mL of fluid per day
• High-output fistulas ----- drain more than 500 mL of fluid per day

55. Pathophysiology
• Enterovesicular fistulas often cause recurrent urinary tract infections.
• The drainage emanating from enterocutaneous fistulas are irritating
to the skin and cause excoriation.
• The loss of enteric luminal contents, particularly from high-output
fistulas originating from the proximal small intestine, results in
dehydration, electrolyte abnormalities, and malnutrition.

56. Clinical Presentation
• Iatrogenic enterocutaneous fistulas usually become clinically evident
between the fifth and tenth postoperative days.
• Fever, leukocytosis, prolonged ileus, abdominal tenderness, and
wound infection are the initial signs.
• The diagnosis becomes obvious when drainage of enteric material
through the abdominal wound or through existing drains occurs.
• These fistulas are often associated with intra-abdominal abscesses.

57. Diagnosis
• CT scanning following the
administration of enteral
contrast is the most useful initial
test
• Fistulogram
“FRIEND” (Foreign body within
the fistula tract, Radiation
enteritis, Infection/Inflammation
at the fistula origin,
Epithelialization of the fistula
tract, Neoplasm at the fistula
origin, Distal obstruction of the
intestine

58. Therapy
• The treatment of enterocutaneous fistulas should proceed through an
orderly sequence of steps.
1. Stabilization.
• Fluid and electrolyte resuscitation is begun.
• Nutrition is provided, usually through the parenteral route initially.
• Sepsis is controlled with antibiotics and drainage of abscesses.
• The skin is protected from the fistula effluent with ostomy appliances or fistula drains.
2. Investigation. The anatomy of the fistula is defined.
3. Decision. The available treatment options are considered, and a timeline
for conservative measures is determined.
4. Definitive management. This entails the surgical procedure and requires
appropriate preoperative planning and surgical experience.
5. Rehabilitation.

59. • Timing of Surgical Intervention.
• Most surgeons would pursue 2 to 3 months of conservative therapy before
considering surgical intervention.
• This approach is based on evidence that 90% of fistulas that are going to close
do so within 5 weeks and also that surgical intervention after this time period
is associated with better outcomes and lower morbidity.

60. • Outcomes
• Over 50% of intestinal fistulas close spontaneously

61. RADIATION ENTERITIS
• An undesired side effect of radiation therapy
• Two distinct syndromes:
• Acute 75%
• Chronic 5-15%
• Pathophysiology
• Radiation induces cellular injury directly and through the generation of free
radicals.
• Villus blunting and a dense infiltrate of leukocytes and plasma cells within the
crypts.
• With severe cases, mucosal sloughing, ulceration, and hemorrhage are observed.

62. • Risk factors
• Hypertension, diabetes mellitus, coronary artery disease, and restricted mobility
of the small intestine due to adhesions
• Concomitant administration of chemotherapeutic agent
• Chronic radiation enteritis is characterized by a progressive occlusive vasculitis
• Clinical Presentation
• Acute :-
• Nausea, vomiting, diarrhea, and crampy abdominal pain
• Transient and subside after the discontinuation of radiation therapy
• Chronic :-
• Become evident within 2 years
• Partial small bowel obstruction, with nausea, vomiting, intermittent abdominal
distention, crampy abdominal pain, and weight loss being the most common
symptoms
• Terminal ileum is the most frequently affected
• Intestinal hemorrhage, and abscess or fistula formation

63. • No specific investigation
• USG or CT imaging to rule out acute abdominal syndrome
• Enteroclysis is the most accurate imaging test for diagnosing chronic
radiation enteritis

64. Therapy
• Most cases of acute radiation enteritis are self-limited.
• Supportive therapy, including the administration of antiemetics, is
usually sufficient.
• Patients with diarrhea-induced dehydration may require hospital
admission and parenteral fluid administration.
• Rarely are symptoms severe enough to necessitate reduction in or
cessation of radiation therapy.
• Chronic
• Surgery for high grade obstruction, perforation, hemorrhage,
intra-abdominal abscesses, and fistulas

65. MECKEL’S DIVERTICULUM

66. • Most prevalent congenital anomaly of the GI tract
• Affect 2% of the general population.
• True diverticula ( all of the layers found in normal small intestine).
• Usually found in the ileum within 100 cm of the ileocecal valve
• Approximately 60% of Meckel’s diverticula contain heterotopic
mucosa, of which over 60% consist of gastric mucosa.
• Pancreatic acini are the next most common; others include Brunner’s
glands, pancreatic islets, colonic mucosa, endometriosis, and
hepatobiliary tissues

67. • “Rule of two’s”:
• 2% prevalence,
• 2:1 male predominance,
• 2 feet proximal to the ileocecal valve in adults
• Symptomatic are under 2 years of age.

68. Pathophysiology
• During the eighth week of gestation, the omphalomesenteric (vitelline)
duct normally undergoes obliteration.
• Failure or incomplete vitelline duct obliteration results in a spectrum of
abnormalities, the most common of which is Meckel’s diverticulum.
• Other abnormalities include omphalomesenteric fistula, enterocyst, and a
fibrous band connecting the intestine to the umbilicus.
• A remnant of the left vitelline artery can persist to form a mesodiverticular
band tethering a Meckel’s diverticulum to the ileal mesentery.
• Bleeding associated with Meckel’s diverticulum is usually the result of ileal
mucosal ulceration that occurs adjacent to acid-producing, heterotopic
gastric mucosa located within the diverticulum.

69. • Intestinal obstruction associated with Meckel’s diverticulum can
result from several mechanisms:
1. Volvulus of the intestine around the fibrous band attaching the diverticulum
to the umbilicus
2. Entrapment of intestine by a mesodiverticular band
3. Intussusception with the diverticulum acting as a lead point
4. Stricture secondary to chronic diverticulitis
Meckel’s diverticula can be found in inguinal or femoral hernia sacs (known as
Littre’s hernia)

71. Clinical Presentation
• Asymptomatic unless associated with complications.
• The lifetime incidence rate of complications is approximately 4-6%.
• Bleeding, intestinal obstruction, and diverticulitis
• Bleeding is the most common presentation in children with Meckel’s
diverticula
• Intestinal obstruction is the most common presentation in adults with
Meckel’s diverticula

72. Diagnosis
• Most are discovered incidentally on radiographic imaging, during endoscopy, or
at the time of surgery.
• In the absence of bleeding, Meckel’s diverticula rarely are diagnosed prior to
the time of surgical intervention.
• The sensitivity of CT scanning for the detection of Meckel’s diverticula is too
low to be clinically useful.
• Enteroclysis is associated with an accuracy of 75% but is usually not applicable
during acute presentations of complications related to Meckel’s diverticula.
• Radionuclide scans (99mTc-pertechnetate) can be helpful in the diagnosis of
Meckel’s diverticulum; however, this test is positive only when the diverticulum
contains associated ectopic gastric mucosa that is capable of uptake of the
tracer
• Angiography can localize the site of bleeding during acute hemorrhage related
to Meckel’s diverticula.

73. Therapy
• The surgical treatment of symptomatic Meckel’s diverticula should
consist of diverticulectomy with removal of associated bands
connecting the diverticulum to the abdominal wall or intestinal
mesentery.
• If the indication for diverticulectomy is bleeding, segmental resection
of ileum that includes both the diverticulum and the adjacent ileal
peptic ulcer should be performed.
• Segmental ileal resection may also be necessary if the diverticulum
contains a tumor or if the base of the diverticulum is inflamed or
perforated.

74. • The management of incidentally found (asymptomatic) Meckel’s
diverticula is controversial

75. ACQUIRED DIVERTICULA

76. • False diverticula (walls consist of mucosa and submucosa but lack a
complete muscularis)
• More common in the duodenum
• Tend to be located near the ampulla; such diverticula are known as
periampullary, juxta-papillary, or peri-vaterian diverticula
• The mean age of diagnosis ranges from 56 to 76 years

78. Pathophysiology
• Hypothesized to be related to acquired abnormalities of intestinal
smooth muscle or dysregulated motility, leading to herniation of
mucosa and submucosa through weakened areas of muscularis.

79. Clinical Presentation
• Asymptomatic unless associated with complications.
• Complication rate is 6 - 10%
• Complications are - intestinal obstruction, diverticulitis, hemorrhage,
perforation, and malabsorption.
• Periampullary duodenal diverticula may be associated with
choledocholithiasis, cholangitis, recurrent pancreatitis, and sphincter of
Oddi dysfunction.
• Symptoms such as intermittent abdominal pain, flatulence, diarrhea,
and constipation are reported to be present in 10% to 30% of patients
with jejunoileal diverticula.

80. Diagnosis
• Most acquired diverticula are discovered incidentally on radiographic
imaging, during endoscopy, or at the time of surgery.
• On ultrasound and CT scanning, duodenal diverticula may be
mistaken for pancreatic pseudocysts and fluid collections, biliary
cysts, and periampullary neoplasms.
• Enteroclysis is the most sensitive test for detecting jejunoileal
diverticula

81. Therapy
• Asymptomatic acquired diverticula should be left alone.
• Bacterial overgrowth associated with acquired diverticula is treated
with antibiotics.
• Other complications, such as bleeding and diverticulitis, are treated
with segmental intestinal resection for diverticula located in the
jejunum or ileum

82. MESENTERIC ISCHEMIA

83. • Two distinct clinical syndromes:
• Acute mesenteric ischemia
• Chronic mesenteric ischemia--- results from atherosclerotic lesions
• Four distinct pathophysiologic mechanisms can lead to acute mesenteric
ischemia:
1.Arterial embolus -- most common cause
2.Arterial thrombosis
3.Vasospasm (also known as nonocclusive mesenteric ischemia [NOMI])
4.Venous thrombosis
Acute mesenteric ischemia can lead to intestinal mucosal sloughing within 3 hours of
onset and full-thickness intestinal infarction by 6 hours.

84. Clinical presentation
• Severe abdominal pain, out of proportion to the degree of tenderness
on examination, is the hallmark of acute mesenteric ischemia,
regardless of the pathophysiologic mechanism.
• The pain is typically perceived to be colicky and most severe in the
mid abdomen.
• Associated symptoms can include nausea, vomiting, and diarrhea.
• Physical findings are characteristically absent early in the course of
ischemia.
• With the onset of bowel infarction, abdominal distension, peritonitis,
and passage of bloody stools occur.

85. • Chronic mesenteric ischemia presents insidiously.
• Postprandial abdominal pain is the most prevalent symptom,
producing a characteristic aversion to food (“food fear”) and weight
loss.
• These patients are often thought to have a malignancy and suffer a
prolonged period of symptoms before the correct diagnosis is made.

86. Small Bowel Perforation

87. • Causes
• GI endoscopy is the most common cause.
• Infections (especially tuberculosis, typhoid, and CMV),
• Crohn’s disease,
• Ischemia,
• Drugs (e.g., potassium- and NSAID-induced ulcers),
• Radiation-induced injury,
• Meckel’s and acquired diverticula,
• Neoplasms (especially lymphoma, adenocarcinoma, and melanoma), and
• Foreign bodies.

88. • CT scanning is the most sensitive test for diagnosing duodenal
perforations
• positive findings include pneumoperitoneum for free perforations, but more
commonly retroperitoneal air, contrast extravasation, and paraduodenal fluid
collections.
• True cases of retroperitoneal perforations of the duodenum can be
managed nonoperatively, in the absence of progression and sepsis
• Intraperitoneal duodenal perforations require surgical repair with
pyloric exclusion and gastrojejunostomy or tube duodenostomy.
• Endoscopic repair techniques

89. Jejunum and ileum perforation
• Occurs into the peritoneal cavity
• Causes overt symptoms and signs
• Abdominal pain
• Tenderness
• Distention
• Fever
• Tachycardia
• Plain abdominal radiographs may reveal free intraperitoneal air.
• CT scan if no obvious cause if found.
• Jejunal and ileal perforations require surgical repair or segmental
resection.

91. SHORT BOWEL SYNDROME

92. • Arbitrarily defined as the presence of less than 200 cm of residual small
bowel in adult patients.
• A functional definition, in which insufficient intestinal absorptive capacity
results in the clinical manifestations of diarrhea, dehydration, and
malnutrition, is more broadly applicable
• In adults, the most common etiologies of short bowel syndrome are acute
mesenteric ischemia, malignancy, and Crohn’s disease.
• In pediatric patients, intestinal atresias, volvulus, and necrotizing
enterocolitis
• 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.
• The ileo-caecal valve used to be considered important with regard to
preservation of absorptive function.

93. Pathophysiology
• Resection of less than 50% of the small intestine is generally well tolerated.
• Clinically significant malabsorption occurs when greater than 50% to 80% of
the small intestine has been resected.
• Among adult patients who lack a functional colon, lifelong TPN dependence is
likely to persist if there is less than 100 cm of residual small intestine.
• Among adult patients who have an intact and functional colon, lifelong TPN
dependence is likely to persist if there is less than 60 cm of residual small
intestine.
• Among infants with short bowel syndrome, weaning from TPN dependence has
been achieved with as little as 10 cm of residual small intestine.
• Residual bowel length is not the only factor predictive of achieving
independence from TPN (enteral autonomy), however. Other determinants of
the severity of malabsorption include the presence or absence of an intact
colon, as indicated earlier.

94. Therapy
• Medical Therapy
• Repletion of fluid and electrolytes lost in the severe diarrhea
• TPN
• Enteral nutrition should be gradually introduced, once ileus has resolved
• High-dose histamine-2 receptor antagonists or proton pump inhibitors
should be administered to reduce gastric acid secretion.
• Antimotility agents, such as loperamide hydrochloride or diphenoxylate,
may be administered to delay small-intestinal transit.
• Octreotide can be administered to reduce the volume of GI secretions
• Liver failure is a significant source of morbidity and often leads to liver
transplantation

95. • Intestinal lengthening operation
• Longitudinal intestinal lengthening and tailoring (LILT) procedure
• Serial transverse enteroplasty procedure (STEP).
• Intestinal Transplantation
• Specific complications for which intestinal transplantation is indicated include
• (a) impending or overt liver failure,
• (b) thrombosis of major central veins,
• (c) frequent episodes of catheter-related sepsis, and
• (d) frequent episodes of severe dehydration

96. Serial transverse enteroplasty (STEP)
procedure

97. Coeliac disease

98. • Most common cause of malabsorption in the UK.
• Characterized by a hypertrophic small bowel mucosa with atrophic
villi and deep crypts.
• Loss of surface area and brush border enzymes
• Caused by an abnormal immune response to gluten, a cereal protein,
although the exact mechanism remains unclear.
• More common in first-degree relatives.
• Has an association with HLA B8

99. • Steatorrhoea and growth retardation in children.
• In adults, diarrhoea and weight loss but many patients simply present
with an iron deficiency anaemia.
• Some patients develop a characteristic skin rash (dermatitis
herpetiformis)
• The diagnosis is 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

100. • 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.
• 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.

101. STOMAS

102. • An artificial opening
made in the colon (or
small intestine) to divert
faeces and flatus out-
side the abdomen.
• May be
• Temporary
• Permanent

103. Loop ileostomy
• Used for defunctioning a low rectal anastomosis or an ileal pouch.
• A knuckle of ileum is exteriorised through a skin trephine in the right
iliac fossa.
• The advantages of a loop ileostomy over a loop colostomy
• The ease with which the bowel can be brought to the surface and the relative
absence of odour.
• Care is needed when the ileostomy is closed, so that suture line obstruction
does not occur.
• Closure of a loop ileostomy can be a technically challenging procedure,
particularly if there are dense adhesions resulting from previous surgery.

104. End ileostomy
• Formed after a subtotal colectomy without anastomosis, when it may later be
reversed, or may be permanent after a panproctocolectomy.
• The ileum is normally brought through the rectus abdominis muscle.
• Careful attention to the terminal ileal mesentery should be taken to ensure that it is
not too bulky.
• The use of a spout was originally described by Bryan Brooke; this should project some
2–4 cm from the skin surface
• A disposable appliance is placed over the ileostomy so that it is a snug fit at skin level.
• There may be an ‘ileostomy flux’ while the ileum adapts to the loss of the colon.
• While ileostomy output can amount to 4 or 5 litres per day, losses of 1–2 litres are
more common.
• A consistent ileostomy output in excess of 1.5 litres is usually associated with
dehydration and sodium depletion in the absence of intravenous therapy.
• Complications of an ileostomy include prolapse, retraction, stenosis, bleeding, fistula
and parastomal hernia.

105. Stoma bags and appliances
• Stoma output is collected in disposable adhesive bags.
• Ileostomy appliances tend to be drainable bags, which are left in
place for 48 hours,
• While colostomy appliances are simply changed two or three times
each day.
• A wide range of such bags is currently available.
• Many now incorporate an adhesive backing, which can be left in place
for several days.

107. THANK YOU 