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Small Intestine
Dr Simba Fidel, MCS 2021
Overview
• Introduction
• Anatomy & Physiology
• Small Bowel Pathologies and Management
Introduction
• The small intestine is the “Raison d’être” of the gastrointestinal tract,
as it the principle site for digestion and absorption.
• It is also the body’s largest reservoir of immunologically active and
hormone-producing cells and hence, can be conceptualized as the
largest organ of the immune and endocrine systems,
• It starts from the pylorus and ends at the ileo-cecal valve, and
measures about 7meters.
• It is divided into; the Duodenum, Jejunum and Ileum.
Embryology
• Nearly all of the small intestine is of midgut origin embryologically,
except the proximal duodenum, which develops from the foregut.
• The gut tube initially communicates with the yolk sac,
• The communication between these two structures narrows by the 6th
week to form the vitelline duct.
• During the fifth week of gestation, the developing intestine herniates
out of the coelomic cavity and begins to undergo a counterclockwise
rotation about the axis of the superior mesenteric artery
Gross Anatomy
Duodenum
• The duodenum is divided anatomically into 4 sections;
1. The bulb: It’s attached to he liver by the hepatoduodenal ligament, which
contains the Porta Hepatis.
2. The second portion; Runs caudally and abuts the pancreatic head. Overlies
the IVC and Rt kidney.
3. The 3rd portion runs transversely and posteriorly between the superior
mesenteric vessels(anterior), and the IVC and Aorta(posteriorly).
4. The 4th segment passes through the ligament of Treitz, to continue at the
jejunum.
• It measures about 25cm in length
Duodenum
Arterial Supply
• The proximal portion is supplied
by the Superior
pancreaticoduodenal artery,
derived from the
gastroduodenal artery.
• The distal segments are supplied
by the inferior
pancreaticoduodenal branches
of the SMA
Venous supply
• The drainage follows the
arteries, and the forgut
portion drains into the splenic
vein,
• The midgut drains into the
SMV.
• Lymphatics follow the venous
drainage.
Jejunum
• 2nd portion of the small intestine.
Entirely intraperitoneal.
• There is no transition line btn the
duodenum and jejunum, but the
jejunum is wider with a thicker wall
and less mesenteric fat.
• Arterial and venous systems are
through the jejunal branches of the
SMA and SMV.
Ileum
• 3rd portion of the small intestine
• Entirely intraperitoneal
• Arterial supply is via the ileal
branches of the SMA
• Venous drainage is through the
ileal tributaries to the SMV then
to the portal vein.
Histology
• Mucosa: composed of columnar
epithelium, supporting vessels and
smooth muscle.
• Submucosa: composed of dense
connective tissue, leukocytes, and
fibroblasts.
• Muscularis Propria - outer
longitudinal and inner circular
layer of smooth muscle
Histology
• Serosa - single layer of
mesothelial cells that forms the
peritoneum that covers the
bowel.
• Circular folds known as plicae
circulares condense the length
of the intestine like a spring.
• The plicae contain villi, or
mucosal folds, that project into
the lumen, which contain
microvilli
Physiology
Absorption and Digestion
• Water:
• The daily amount of fluid that
passes through the small intestine
is 9-10 liters per day.
• over 80% of this volume is
reabsorbed, only about 1500 mL
of fluid enters the large bowel.
• absorption occurs across the
intestinal epithelial cells, known as
the “transcellular pathway”
Physiology
Electrolytes
• The small intestine absorbs a
variety of electrolytes. One of
the most important is sodium
• Sodium absorption occurs by
passive diffusion along the
gradient.
• Sodium may diffuse alone or
through cotransport with
glucose or amino acids
Physiology
Physiology
Physiology
Physiology
• Absorption of Other Substances including;
• Glutamine (Amino acid); main source of enterocyte energy
• Reabsorption of Bile Salts
• Vitamins
• B12 (cobalamine)
• Fat soluble vitamins (A,D,E,K)
Physiology
Immune and Barrier functions;
• One of the important functions of the small bowel is to manage the
complex ecosystem of the gut microbiome by acting as a barrier to
pathogens and facilitating symbiosis with beneficial bacteria.
• The histologic structure of the enterocytes is impermeable to bacteria
and potentially harmful macromolecules.
• Gut-associated lymphoid tissues (GALT). The lymphoid tissue of the
small intestine contains a variety of cells involved in the detection and
destruction of pathogens. These celles are found in the Peyer’s
patches
Endocrine Function
Pathologies
Small Bowel Obstruction (SBO);
• The most common etiologies vary from region to region.
• In the west, 75% of admissions for SBO are due to adhesions.
• In sub-Saharan Africa, adhesions make up only about 20 to 25% in
some series.
• Other common reported causes of small bowel obstruction in sub-
Saharan Africa are small bowel volvulus, ileal knotting, ileosigmoid
knotting (or compound volvulus), and intestinal parasites
SBO
Clinical Presentation
• Abdominal pain
• Vomiting
• Abdominal distention
Diagnosis
• Plain upright radiograph;
• distended loops of small bowel (>3cm), air-fluid levels, and a paucity of gas in
the colon
• plain abdominal films are not perfect and only have a sensitivity and
specificity of 67% and 83%, respectively.
SBO
• CT Abdomen
SBO
Small Bowel Follow-Through
(SBFT)
• the patient is most commonly
given 100 mL of water-soluble
contrast, such as Gastrografin.
• imaging is performed after a few
hours (4-6), and then at 24hrs if
the contrast is not seen in the
colon initially.
SBO
Several findings on CT scan are
suggestive of intestinal infarction.
• The presence of greater than 500
mL of free fluid or
• fluid that is dense (>10HU)
• edema in the mesentery,
• decreased contrast enhancement
of the bowel wall,
• thickened loops of small bowel,
• pneumatosis intestinalis (air
within the bowel wall),
• free air, and
• portal venous gas.
SBO
Management
• Initial management begins with correcting fluid and electrolyte losses.
• Regardless of whether an operative or nonoperative approach is planned,
this volume deficit needs to be rapidly replaced.
• Patients with peritonitis due to bowel infarction or perforation may present
with septic shock. These patients may need vasopressor support, antibiotics,
and operative exploration.
• Decision for operative vs no-operative treatment will be guided by the
presumed or confirmed etiology of the obstruction, and whether or not there
is suspicion for bowel ischemia or perforation.
• Patients with partially obstructing etiologies that are amenable to
medical therapy can also be managed nonoperatively, such as
infection with Ascaris or Crohn’s disease.
• However, patients with obstructing processes that will not
spontaneously resolve are ill-suited for nonoperative
management. Such pathologies include obstructing masses, volvulus,
or hernias.
Non Operative Management:
• NPO
• Insert an NGT
• IV fluids and monitoring electrolytes
• Trends of WBC counts may be helpful when clinical exams are
equivocal
• SBFT may help make the decision to operate in some circumstances.
• Data suggest that complication rates of operative intervention rise
when nonoperative therapy is extended beyond 72 hours
Operative Management;
• Before an operation, patients should be well resuscitated and major
electrolyte derangements corrected.
• Placement of an NGT
• Broad spectrum antibiotics
• Laparoscopic surgery is most preferred.
• An open operation is safe in the absence of skill or equipement for
laparoscopic surg.
Ileus
• Adynamic ileus is a disorder resulting in impaired motility of the small
intestine.
• Ileus is a secondary process to some other systemic or intra-
abdominal process;
• Sepsis from any cause,
• electrolyte abnormalities,
• medications, and
• spinal cord injury
• Post laparotomy complication
Ileus
• On plain abdominal films, there
is often distension of both the
small and large bowel in patients
with ileus.
• CT is very helpful when the
diagnosis remains uncertain
Ileus
Management;
• Supportive care.
• Correction of electrolyte imbalances
• NGT for severely distended bowels, with vomiting
Typhoid (Enteric Fever)
• caused by the bacteria Salmonella enterica serotype Typhi (formerly
called Salmonella typhi)
• If not treated early, the bacteria can proliferate in the Peyer’s patches,
located mostly in the terminal ileum, & cause full thickness necrosis.
Typhoid (Enteric Fever)
Clinical Presentation;
• it is most common in children (5-14 years old) in endemic areas.
• Clinical symptoms usually start 5 to 21 days after ingesting the bacteria.
• Initial symptoms are fever (week one), followed by abdominal pain (week
two), if not yet started on antibiotics, will complicate with diffuse peritonitis
and abdominal distention (week 3).
• Patients with acute acalculous cholecystitis secondary to typhoid are
often not identified preoperatively.
Typhoid (Enteric Fever)
Diagnosis;
• The diagnosis of typhoid perforation can often be made by history,
physical exam, and ultrasound evidence of particulate-free fluid
alone.
• On lab evaluation, the patient often will have anemia, leukocytosis or
leukopenia, and often, hyponatremia.
• Blood cultures are the most accurate clinical test to diagnose patients
with typhoid and are positive in 50 to 70% of typhoid patients
Typhoid (Enteric Fever)
Management;
• Non-operative: Uncomplicated typhoid fever can be treated with a
variety of antibiotic regimens.
• Operative mgt: Most patients with perforated typhoid have a single
perforation in the terminal ileum that can be debrided and closed
primarily.
• The number and location of the perforations along with the patient’s clinical
status and degree of malnutrition affect the decision for primary repair.
Tuberculosis of the Small Intestine
• The most common site of gastrointestinal TB is the ileocecal region
followed by the jejunum.
• The clinical presentation can mimic Crohn's as patients often present
with obstructive symptoms due to stricturing and thickening of the
bowel wall.
• Imaging, may include plain radiographs, contrast studies, or CT scans
may show strictures and/or bowel wall thickening as well as
associated lymphadenopathy.
• For symptomatic strictures, stricturoplasty is typically the procedure
of choice. For perforations, limited resection and anastomosis is
performed.
Small Bowel Neoplasms
• Small bowel neoplasms are
relatively rare and can be
difficult to diagnose.
• Most symptomatic patients will
present with symptoms of
obstruction; however, a minority
can present with bleeding
Crohn’s Disease
• CD is a spectrum of inflammatory bowel disease characterized by
transmural inflammation of the GI tract.
• It commonly affects the ileum but can still affect any part of the GI
tract from the mouth to the anus.
• It is most common in the northern hemisphere but is relatively
uncommon in sub-Saharan Africa.
Crohn’s Disease
Presentation;
• There are certain patterns of disease that can be identified:
• Fibrostenotic disease - characterized by segmental stenosis of involved areas,
most commonly the ileum.
• Fistulizing disease - characterized by the development of fistula between GI
segments or to the skin. The location of the fistula determines the
presentation.
• Aggressive inflammatory disease - characterized by abdominal pain, weight
loss, and diarrhea. This form can be difficult to differentiate from infectious
causes of enteritis.
Crohn’s Disease
Diagnosis;
• The diagnosis is based on
pathology, which shows
transmural inflammation and
exclusion of other pathologies.
Crohn’s Disease
Treatment;
• Medical therapy is aimed at treating and preventing acute flares of Crohn’s
disease and is preferred over surgical therapy
• These include;
• Anti-Inflammatory medications; e.g Salicylates and Glucocorticoids
• Immune Modulators; e.g Thiopurine antimetabolites and biologic therapies
• Surgery is indicated in symptomatic patients with segmental disease who fail
to respond to medical intervention
Mesenteric Ischemia
• Mesenteric ischemia is a situation in which blood supply to the small
intestine is impaired.
• Because perfusion to the bowel is from the outer layers inward to the
mucosa, the mucosa is the least well-perfused part of the bowel wall
and the first layer to become ischemic.
• Ischemia of the small intestine manifests as two basic clinical
presentations: acute and chronic.
Acute Mesenteric Ischemia
Four pathophysiologic processes can lead to acute mesenteric
ischemia,
1. Emboli; accounts for about 50% of cases.
• It is often caused by emboli from a cardiac source, such as atrial fibrillation or
valvular disease, but can also originate from aneurysm sacs.
• A majority of SMA emboli will either lodge around the branch point of the
middle colic artery (40%) or go to more distal branches (45%)
Acute Mesenteric Ischemia
2. Acute thrombosis; Thrombosis is usually associated with proximal
SMA atherosclerotic disease
3. Mesenteric Venous thrombosis: Acute venous thrombosis of the
SMV (or its mesenteric branches) or the portal vein can lead to
ischemia due to resulting venous hypertension in the bowel wall.
4. Non-Occlusive Mesenteric Ischemia; there is no physical occlusion,
either of the arteries or the veins.
• Instead this ischemic process results from any low-flow state, which globally
reduces blood flow to the intestines
Acute Mesenteric Ischemia
Presentation;
• The classic presentation is severe, acute abdominal pain, which is perceived
by the patient, that is out of proportion to the degree of abdominal
tenderness on the physical exam.
• Peritonitis (late finding)
• Bloody bowel movement
• Abdominal distention
• CT with IV contrast helps determine the patency of mesenteric
vasculature, assess the bowel for evidence of ischemia.
Acute Mesenteric Ischemia
• Treatment;
• Resuscitation should be
performed in all patients with
mesenteric ischemia.
• Intravenous fluids should be
administered but are especially
important in patients with NOMI.
• Antibiotics are administered,
which helps to reduce bacterial
translocation from the bowel.
Chronic Mesenteric Ischemia
• Chronic mesenteric ischemia is typically caused by atherosclerotic
plaque at the origin of the mesenteric vasculature
• Because intestinal oxygen demands are highest postprandially,
patients will experience pain after eating, resulting in “food fear,”
• Treatment options include arterial bypass and endovascular stenting.
Enterocutaneous Fistula
• Fistulas are abnormal connections between two epithelial surfaces.
• Enterocutaneous fistulas (ECF) are commonly iatrogenic (75-85%) and
are the most common type of small bowel fistula.
• Both an anastomotic leak, and an ECF, indicate that there has been
disruption of the bowel wall.
• An anastomotic leak is usually contained within the abdominal
peritoneal cavity and occurs within a few days to a week after surgery
ECF
Etiology;
• Iatrogenic (most common)
• Crohn’s disease
• Malignancies
• Radiation
• Trauma
• TB
• Foreign bodies
ECF
• fistulas are classified by their
output;
I. Low output; <200ml/day
II. Moderate output; 200-
500ml/day
III. High Output; >500ml/day
ECF
Management
• Stabilization
• Nutrition
• Wound care
• Investigations
• Definitive management.
Small Bowel Diverticula
• Small bowel diverticula occur in
as many as 6% of patients
evaluated with contrast studies.
• small bowel diverticula are false
diverticula, meaning they are
herniations of the mucosa and
submucosa
Small Bowel Diverticula
• Approximately 50% of small
bowel diverticula occur in the
duodenum making this the most
common site in the small
intestine.
• Acquired jejunoileal diverticula
make up 25% of small bowel
diverticula and likely result from
uncoordinated small bowel
motility
Meckel’s Diverticulum
• These are congenital, true diverticula of the ileum that result from
failure of obliteration of the omphalomesenteric duct during
gestational development.
• Account for 25% of all small bowel diverticula.
• Found in 2% of the population
• Children are more likely than adults to develop symptoms from a
Meckel’s diverticulum
Meckel’s Diverticula
• Meckel's diverticula are often characterized by the Rule of 2s
• occur in 2% of the population
• typically present by the age of 2
• are 2 inches (5 cm) long
• are 2 feet (60 cm) from the ileocecal valve
• 2/3 have ectopic mucosa
• 2 types of ectopic tissue are commonly present (gastric and pancreatic)
• 2% become symptomatic
Meckel’s Diverticula
• Surgical treatment is resection of
the diverticulum at its base or
ileal segmental resection.
• Patients with associated ileal
ulcers or wide-based diverticula
are best treated by segmental
resection.
• Systematic reviews do not
support prophylactic resection of
incidental Meckel’s
References
• COSECSA Module on Small Intestine, MCS 2021
• Schwartz’s Principles of Surgery, 10th Edition
THANK YOU!!

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Small intestine

  • 1. Small Intestine Dr Simba Fidel, MCS 2021
  • 2. Overview • Introduction • Anatomy & Physiology • Small Bowel Pathologies and Management
  • 3. Introduction • The small intestine is the “Raison d’être” of the gastrointestinal tract, as it the principle site for digestion and absorption. • It is also the body’s largest reservoir of immunologically active and hormone-producing cells and hence, can be conceptualized as the largest organ of the immune and endocrine systems, • It starts from the pylorus and ends at the ileo-cecal valve, and measures about 7meters. • It is divided into; the Duodenum, Jejunum and Ileum.
  • 4. Embryology • Nearly all of the small intestine is of midgut origin embryologically, except the proximal duodenum, which develops from the foregut. • The gut tube initially communicates with the yolk sac, • The communication between these two structures narrows by the 6th week to form the vitelline duct. • During the fifth week of gestation, the developing intestine herniates out of the coelomic cavity and begins to undergo a counterclockwise rotation about the axis of the superior mesenteric artery
  • 5.
  • 7. Duodenum • The duodenum is divided anatomically into 4 sections; 1. The bulb: It’s attached to he liver by the hepatoduodenal ligament, which contains the Porta Hepatis. 2. The second portion; Runs caudally and abuts the pancreatic head. Overlies the IVC and Rt kidney. 3. The 3rd portion runs transversely and posteriorly between the superior mesenteric vessels(anterior), and the IVC and Aorta(posteriorly). 4. The 4th segment passes through the ligament of Treitz, to continue at the jejunum. • It measures about 25cm in length
  • 8. Duodenum Arterial Supply • The proximal portion is supplied by the Superior pancreaticoduodenal artery, derived from the gastroduodenal artery. • The distal segments are supplied by the inferior pancreaticoduodenal branches of the SMA Venous supply • The drainage follows the arteries, and the forgut portion drains into the splenic vein, • The midgut drains into the SMV. • Lymphatics follow the venous drainage.
  • 9. Jejunum • 2nd portion of the small intestine. Entirely intraperitoneal. • There is no transition line btn the duodenum and jejunum, but the jejunum is wider with a thicker wall and less mesenteric fat. • Arterial and venous systems are through the jejunal branches of the SMA and SMV.
  • 10. Ileum • 3rd portion of the small intestine • Entirely intraperitoneal • Arterial supply is via the ileal branches of the SMA • Venous drainage is through the ileal tributaries to the SMV then to the portal vein.
  • 11. Histology • Mucosa: composed of columnar epithelium, supporting vessels and smooth muscle. • Submucosa: composed of dense connective tissue, leukocytes, and fibroblasts. • Muscularis Propria - outer longitudinal and inner circular layer of smooth muscle
  • 12. Histology • Serosa - single layer of mesothelial cells that forms the peritoneum that covers the bowel. • Circular folds known as plicae circulares condense the length of the intestine like a spring. • The plicae contain villi, or mucosal folds, that project into the lumen, which contain microvilli
  • 13. Physiology Absorption and Digestion • Water: • The daily amount of fluid that passes through the small intestine is 9-10 liters per day. • over 80% of this volume is reabsorbed, only about 1500 mL of fluid enters the large bowel. • absorption occurs across the intestinal epithelial cells, known as the “transcellular pathway”
  • 14. Physiology Electrolytes • The small intestine absorbs a variety of electrolytes. One of the most important is sodium • Sodium absorption occurs by passive diffusion along the gradient. • Sodium may diffuse alone or through cotransport with glucose or amino acids
  • 18. Physiology • Absorption of Other Substances including; • Glutamine (Amino acid); main source of enterocyte energy • Reabsorption of Bile Salts • Vitamins • B12 (cobalamine) • Fat soluble vitamins (A,D,E,K)
  • 19. Physiology Immune and Barrier functions; • One of the important functions of the small bowel is to manage the complex ecosystem of the gut microbiome by acting as a barrier to pathogens and facilitating symbiosis with beneficial bacteria. • The histologic structure of the enterocytes is impermeable to bacteria and potentially harmful macromolecules. • Gut-associated lymphoid tissues (GALT). The lymphoid tissue of the small intestine contains a variety of cells involved in the detection and destruction of pathogens. These celles are found in the Peyer’s patches
  • 21.
  • 22. Pathologies Small Bowel Obstruction (SBO); • The most common etiologies vary from region to region. • In the west, 75% of admissions for SBO are due to adhesions. • In sub-Saharan Africa, adhesions make up only about 20 to 25% in some series. • Other common reported causes of small bowel obstruction in sub- Saharan Africa are small bowel volvulus, ileal knotting, ileosigmoid knotting (or compound volvulus), and intestinal parasites
  • 23.
  • 24. SBO Clinical Presentation • Abdominal pain • Vomiting • Abdominal distention Diagnosis • Plain upright radiograph; • distended loops of small bowel (>3cm), air-fluid levels, and a paucity of gas in the colon • plain abdominal films are not perfect and only have a sensitivity and specificity of 67% and 83%, respectively.
  • 26. SBO Small Bowel Follow-Through (SBFT) • the patient is most commonly given 100 mL of water-soluble contrast, such as Gastrografin. • imaging is performed after a few hours (4-6), and then at 24hrs if the contrast is not seen in the colon initially.
  • 27. SBO Several findings on CT scan are suggestive of intestinal infarction. • The presence of greater than 500 mL of free fluid or • fluid that is dense (>10HU) • edema in the mesentery, • decreased contrast enhancement of the bowel wall, • thickened loops of small bowel, • pneumatosis intestinalis (air within the bowel wall), • free air, and • portal venous gas.
  • 28. SBO Management • Initial management begins with correcting fluid and electrolyte losses. • Regardless of whether an operative or nonoperative approach is planned, this volume deficit needs to be rapidly replaced. • Patients with peritonitis due to bowel infarction or perforation may present with septic shock. These patients may need vasopressor support, antibiotics, and operative exploration. • Decision for operative vs no-operative treatment will be guided by the presumed or confirmed etiology of the obstruction, and whether or not there is suspicion for bowel ischemia or perforation.
  • 29. • Patients with partially obstructing etiologies that are amenable to medical therapy can also be managed nonoperatively, such as infection with Ascaris or Crohn’s disease. • However, patients with obstructing processes that will not spontaneously resolve are ill-suited for nonoperative management. Such pathologies include obstructing masses, volvulus, or hernias.
  • 30. Non Operative Management: • NPO • Insert an NGT • IV fluids and monitoring electrolytes • Trends of WBC counts may be helpful when clinical exams are equivocal • SBFT may help make the decision to operate in some circumstances. • Data suggest that complication rates of operative intervention rise when nonoperative therapy is extended beyond 72 hours
  • 31. Operative Management; • Before an operation, patients should be well resuscitated and major electrolyte derangements corrected. • Placement of an NGT • Broad spectrum antibiotics • Laparoscopic surgery is most preferred. • An open operation is safe in the absence of skill or equipement for laparoscopic surg.
  • 32. Ileus • Adynamic ileus is a disorder resulting in impaired motility of the small intestine. • Ileus is a secondary process to some other systemic or intra- abdominal process; • Sepsis from any cause, • electrolyte abnormalities, • medications, and • spinal cord injury • Post laparotomy complication
  • 33. Ileus • On plain abdominal films, there is often distension of both the small and large bowel in patients with ileus. • CT is very helpful when the diagnosis remains uncertain
  • 34. Ileus Management; • Supportive care. • Correction of electrolyte imbalances • NGT for severely distended bowels, with vomiting
  • 35. Typhoid (Enteric Fever) • caused by the bacteria Salmonella enterica serotype Typhi (formerly called Salmonella typhi) • If not treated early, the bacteria can proliferate in the Peyer’s patches, located mostly in the terminal ileum, & cause full thickness necrosis.
  • 36. Typhoid (Enteric Fever) Clinical Presentation; • it is most common in children (5-14 years old) in endemic areas. • Clinical symptoms usually start 5 to 21 days after ingesting the bacteria. • Initial symptoms are fever (week one), followed by abdominal pain (week two), if not yet started on antibiotics, will complicate with diffuse peritonitis and abdominal distention (week 3). • Patients with acute acalculous cholecystitis secondary to typhoid are often not identified preoperatively.
  • 37. Typhoid (Enteric Fever) Diagnosis; • The diagnosis of typhoid perforation can often be made by history, physical exam, and ultrasound evidence of particulate-free fluid alone. • On lab evaluation, the patient often will have anemia, leukocytosis or leukopenia, and often, hyponatremia. • Blood cultures are the most accurate clinical test to diagnose patients with typhoid and are positive in 50 to 70% of typhoid patients
  • 38. Typhoid (Enteric Fever) Management; • Non-operative: Uncomplicated typhoid fever can be treated with a variety of antibiotic regimens. • Operative mgt: Most patients with perforated typhoid have a single perforation in the terminal ileum that can be debrided and closed primarily. • The number and location of the perforations along with the patient’s clinical status and degree of malnutrition affect the decision for primary repair.
  • 39.
  • 40. Tuberculosis of the Small Intestine • The most common site of gastrointestinal TB is the ileocecal region followed by the jejunum. • The clinical presentation can mimic Crohn's as patients often present with obstructive symptoms due to stricturing and thickening of the bowel wall. • Imaging, may include plain radiographs, contrast studies, or CT scans may show strictures and/or bowel wall thickening as well as associated lymphadenopathy. • For symptomatic strictures, stricturoplasty is typically the procedure of choice. For perforations, limited resection and anastomosis is performed.
  • 41. Small Bowel Neoplasms • Small bowel neoplasms are relatively rare and can be difficult to diagnose. • Most symptomatic patients will present with symptoms of obstruction; however, a minority can present with bleeding
  • 42.
  • 43. Crohn’s Disease • CD is a spectrum of inflammatory bowel disease characterized by transmural inflammation of the GI tract. • It commonly affects the ileum but can still affect any part of the GI tract from the mouth to the anus. • It is most common in the northern hemisphere but is relatively uncommon in sub-Saharan Africa.
  • 44. Crohn’s Disease Presentation; • There are certain patterns of disease that can be identified: • Fibrostenotic disease - characterized by segmental stenosis of involved areas, most commonly the ileum. • Fistulizing disease - characterized by the development of fistula between GI segments or to the skin. The location of the fistula determines the presentation. • Aggressive inflammatory disease - characterized by abdominal pain, weight loss, and diarrhea. This form can be difficult to differentiate from infectious causes of enteritis.
  • 45. Crohn’s Disease Diagnosis; • The diagnosis is based on pathology, which shows transmural inflammation and exclusion of other pathologies.
  • 46. Crohn’s Disease Treatment; • Medical therapy is aimed at treating and preventing acute flares of Crohn’s disease and is preferred over surgical therapy • These include; • Anti-Inflammatory medications; e.g Salicylates and Glucocorticoids • Immune Modulators; e.g Thiopurine antimetabolites and biologic therapies • Surgery is indicated in symptomatic patients with segmental disease who fail to respond to medical intervention
  • 47. Mesenteric Ischemia • Mesenteric ischemia is a situation in which blood supply to the small intestine is impaired. • Because perfusion to the bowel is from the outer layers inward to the mucosa, the mucosa is the least well-perfused part of the bowel wall and the first layer to become ischemic. • Ischemia of the small intestine manifests as two basic clinical presentations: acute and chronic.
  • 48. Acute Mesenteric Ischemia Four pathophysiologic processes can lead to acute mesenteric ischemia, 1. Emboli; accounts for about 50% of cases. • It is often caused by emboli from a cardiac source, such as atrial fibrillation or valvular disease, but can also originate from aneurysm sacs. • A majority of SMA emboli will either lodge around the branch point of the middle colic artery (40%) or go to more distal branches (45%)
  • 49. Acute Mesenteric Ischemia 2. Acute thrombosis; Thrombosis is usually associated with proximal SMA atherosclerotic disease 3. Mesenteric Venous thrombosis: Acute venous thrombosis of the SMV (or its mesenteric branches) or the portal vein can lead to ischemia due to resulting venous hypertension in the bowel wall. 4. Non-Occlusive Mesenteric Ischemia; there is no physical occlusion, either of the arteries or the veins. • Instead this ischemic process results from any low-flow state, which globally reduces blood flow to the intestines
  • 50. Acute Mesenteric Ischemia Presentation; • The classic presentation is severe, acute abdominal pain, which is perceived by the patient, that is out of proportion to the degree of abdominal tenderness on the physical exam. • Peritonitis (late finding) • Bloody bowel movement • Abdominal distention • CT with IV contrast helps determine the patency of mesenteric vasculature, assess the bowel for evidence of ischemia.
  • 51. Acute Mesenteric Ischemia • Treatment; • Resuscitation should be performed in all patients with mesenteric ischemia. • Intravenous fluids should be administered but are especially important in patients with NOMI. • Antibiotics are administered, which helps to reduce bacterial translocation from the bowel.
  • 52. Chronic Mesenteric Ischemia • Chronic mesenteric ischemia is typically caused by atherosclerotic plaque at the origin of the mesenteric vasculature • Because intestinal oxygen demands are highest postprandially, patients will experience pain after eating, resulting in “food fear,” • Treatment options include arterial bypass and endovascular stenting.
  • 53. Enterocutaneous Fistula • Fistulas are abnormal connections between two epithelial surfaces. • Enterocutaneous fistulas (ECF) are commonly iatrogenic (75-85%) and are the most common type of small bowel fistula. • Both an anastomotic leak, and an ECF, indicate that there has been disruption of the bowel wall. • An anastomotic leak is usually contained within the abdominal peritoneal cavity and occurs within a few days to a week after surgery
  • 54. ECF Etiology; • Iatrogenic (most common) • Crohn’s disease • Malignancies • Radiation • Trauma • TB • Foreign bodies
  • 55. ECF • fistulas are classified by their output; I. Low output; <200ml/day II. Moderate output; 200- 500ml/day III. High Output; >500ml/day
  • 56. ECF Management • Stabilization • Nutrition • Wound care • Investigations • Definitive management.
  • 57. Small Bowel Diverticula • Small bowel diverticula occur in as many as 6% of patients evaluated with contrast studies. • small bowel diverticula are false diverticula, meaning they are herniations of the mucosa and submucosa
  • 58. Small Bowel Diverticula • Approximately 50% of small bowel diverticula occur in the duodenum making this the most common site in the small intestine. • Acquired jejunoileal diverticula make up 25% of small bowel diverticula and likely result from uncoordinated small bowel motility
  • 59. Meckel’s Diverticulum • These are congenital, true diverticula of the ileum that result from failure of obliteration of the omphalomesenteric duct during gestational development. • Account for 25% of all small bowel diverticula. • Found in 2% of the population • Children are more likely than adults to develop symptoms from a Meckel’s diverticulum
  • 60. Meckel’s Diverticula • Meckel's diverticula are often characterized by the Rule of 2s • occur in 2% of the population • typically present by the age of 2 • are 2 inches (5 cm) long • are 2 feet (60 cm) from the ileocecal valve • 2/3 have ectopic mucosa • 2 types of ectopic tissue are commonly present (gastric and pancreatic) • 2% become symptomatic
  • 61. Meckel’s Diverticula • Surgical treatment is resection of the diverticulum at its base or ileal segmental resection. • Patients with associated ileal ulcers or wide-based diverticula are best treated by segmental resection. • Systematic reviews do not support prophylactic resection of incidental Meckel’s
  • 62. References • COSECSA Module on Small Intestine, MCS 2021 • Schwartz’s Principles of Surgery, 10th Edition

Editor's Notes

  1. The dominant pathway is thought to occur by absorption across the intestinal epithelial cells, known as the “transcellular pathway”. Transcellular absorption is accomplished by various transport proteins and water channels, known as aquaporins, and relies on osmosis as the small intestine absorbs sodium and other solutes.
  2. Gut-associated lymphoid tissues (GALT). The lymphoid tissue of the small intestine contains a variety of cells involved in the detection and destruction of pathogens. Cells involved in detection are found within Peyer’s patches, which are lymphoid nodules within the wall of the ileum, lymph nodes, and other areas of lymphoid tissue. Plasma cells in the lamina propria produce IgA, which aids in the destruction or removal of pathogens.
  3. Placement of a nasogastric tube before surgery will allow for decompression of the fluid-filled stomach and may reduce the probability of aspiration at induction of anesthesia. Even with an NGT in place, induction of anesthesia is best performed in a rapid sequence fashion with minimal bagging. Due to instability or gross intraperitoneal contamination, an ostomy may be performed rather than an anastomosis
  4. It can also result in extraintestinal manifestations of many systems of the body, including the skin (pyoderma gangrenosum or erythema nodosum), joints (arthritis), and liver and biliary tract (autoimmune hepatitis, gallstones, and primary sclerosing cholangitis, though PSC is more common in ulcerative colitis than Crohn's). The incidence of the disease varies dramatically from region to region
  5. Cobblestoning (top picture) and fat creeping (bottom picture) may be findings on surgical pathology in Crohn's disease.
  6. Anti-inflammatory medications are often the first line of treatment: Salicylates: 5-ASA and sulfasalazine are less commonly used in places where newer immune-modulating medications are available. Glucocorticoids: These are typically used short-term to induce remission or to improve the effectiveness of immune-modulating medications. Immune modulators: Thiopurine antimetabolites: Azathioprine and 6-mercaptopurine are the most commonly used immunosuppressants for Crohn's disease. Methotrexate is another antimetabolite that is less commonly used for Crohn's but may be an option in certain situations. Biologic therapies: Infliximab and adalimumab are monoclonal antibodies that inhibit tumor necrosis factor (TNF). Other monoclonal antibodies inhibit other cell molecules and proteins.
  7. The general principle in all patients with acute mesenteric ischemia is resection of nonviable small bowel followed by intervention directed at the exact cause of ischemia. In patients with embolic infarction, the source of the emboli should be located and treated to prevent a recurrence. Full-thickness necrosis of the majority of the small intestine is usually not compatible with survival.
  8. Types of fistulas may include enteroenteric (between two loops of the small bowel), enterocolic (between the small bowel and colon), enterovesical (between the small bowel and bladder), and enterocutaneous (between the small bowel and skin) As we discuss enterocutaneous fistulas, it is important to distinguish between a postoperative anastomotic leak and an enterocutaneous fistula. Both an anastomotic leak, which is an acute phenomenon, and an ECF, which is a subacute or chronic phenomenon, indicate that there has been disruption of the bowel wall. This disruption leads to fluid extravasation from the intestinal lumen. While fistulas can be spontaneous, iatrogenic, or the cause of any of the pathologies discussed below, they often occur postoperatively either from a missed injury to the bowel or from an anastomotic disruption. An anastomotic leak is usually contained within the abdominal peritoneal cavity and occurs within a few days to a week after surgery. It will cause peritonitis and/or create an abscess. Once there is leakage of bowel contents from a skin incision or drain site, which will usually occur within 5 to 10 days after surgery, this now constitutes an enterocutaneous fistula. 
  9. Management focuses on broad principles as listed below. Stabilization. Patients with enterocutaneous fistulas can present with life-threatening hypovolemia, electrolyte disorders, and sepsis. The first priority of management is therefore timely identification and treatment of these conditions. Fluid resuscitation with crystalloids can promptly restore intravascular volume. Electrolyte disturbances of sodium and potassium are common and should be corrected. Patients with enterocutaneous fistulas are at risk for wound infection, intra-abdominal abscesses, and sepsis. Sources of infection should be urgently treated with appropriate antibiotic therapy and drainage or debridement as indicated. Abdominal ultrasound and CT are useful in identifying intra-abdominal sources of infection and should be performed to rule out an abscess. Nutrition. Patients with colocutaneous fistulas, distal small bowel fistulas, and low output fistulas are suitable for enteral feedings. Patients with high output fistulas, especially if in a more proximal location, are typically started on parenteral nutrition if available. Total parenteral nutrition (TPN) is most useful as a bridge to enteral feeds while stabilizing the patient and controlling the fistula with wound care. Trials of oral feeding are encouraged, and antimotility agents may help control fistula output. Further, the output of the fistula should be quantified before beginning feeds and after to determine if there is a substantial increase in output once oral feeds are initiated. Wound care. The goals of wound care are to control intestinal contentoutput and to protect the surrounding skin. Wounds can vary in size and volume of effluent that can sometimes make this stage of management challenging. Use of negative pressure therapy or large stoma bags can be helpful. Investigations. Identifying the location of the fistula is helpful in planning treatment. Knowledge of operations performed and the location of anastomoses is important in this step. CT imaging with enteric contrast is frequently helpful and can rule out complicating features such as a bowel obstruction or abscess. Definitive management. Nearly 70% of enterocutaneous fistulas will close spontaneously, though this is dependent on cause and location within the small intestine. Typically, if a fistula is going to close spontaneously it will do so within 5 weeks.  The mnemonic SNAP may help you remember the above principles: S - stabilization, sepsis, and skin care; N - nutrition; A - defining the anatomy; and, P - the definitive procedure.
  10. Meckel’s diverticula are congenital, true diverticula of the ileum that result from failure of obliteration of the omphalomesenteric duct during gestational development. In contrast to acquired duodenal and jejunoileal diverticula, Meckel’s diverticula develop on the antimesenteric side of the ileum. These diverticula account for 25% of all small bowel diverticula, and are found in 2% of the population. Like other diverticula, Meckel’s diverticula can cause infection (diverticulitis), perforation, obstruction, and bleeding. However, bleeding and obstruction are the most common symptoms. Children are more likely than adults to develop symptoms from a Meckel’s diverticulum. One of the unique findings in Meckel’s diverticula is the presence of ectopic tissue. Sixty percent will have ectopic tissue within the diverticula, with gastric and pancreatic tissue being the most common type. Ectopic tissue can be identified intraoperatively by palpating mass-like tissue within the diverticulum. Acid or enzymatic production by this ectopic tissue can lead to ulceration and bleeding of the adjacent ileal mucosa.