1. IschemIc
bowel
dIsease
Lecture 11, 12
Vascular disorders

2. Vascular disorders
•Ischemic Bowel Disease
•Angiodysplasia
•Hemorrhoids

3. Definition
Ischemic bowel disease results from
inadequate flow of oxygenated
blood to the intestines.
• The extent of ischemic bowel disease can range
from mild to severe based on the amount of
damage from lack of oxygenated blood.

4. • Ischemic lesions may be restricted to the
•Small intestine mesenteric ischemia
•Large intestine ischemic colitis or
•Both enterocolitis

5. Blood Supply
• The majority of the GI tract is supplied by the
celiac, superior mesenteric, and
inferior mesenteric arteries.
• As they approach the intestinal wall the superior
and inferior mesenteric arteries ramify
into the mesenteric
arcades.

6. • Interconnections between arcades, as well as
collateral supplies from the proximal celiac
and distal pudendal and iliac circulations,
make it possible for the small intestine and
colon to tolerate slowly progressive loss of
the blood supply from one artery.
• In contrast, acute compromise of any major
vessel can lead to infarction of several
meters of intestine.

7. Levels of infarction
• Transmural infarction involving all layers of the gut.
• Mural infarction– mucosa & submucosa
• Mucosal infarction- mucosa
Mural-Of Wall

8. • Transmural infarction is caused by acute
occlusion of a major mesenteric artery.
• Mural or mucosal infarction more often results
from either physiologic hypoperfusion or more
localized anatomic defects and may be
acuteor chronic.

9. Predisposing conditions
1. Arterial thrombosis
2. Arterial embolism Occlusive
3. Venous thrombosis- less frequent
cause
4. Nonoclusive ischemia
5. Miscellaneous
}

10. Arterial thrombosis
• Severe atherosclerosis
• Systemic vasculitis
• Dissecting aneurism An aneurysm in which the wall of an artery rips (dissects) longitudinally
• Angiographic procedures
• Aortic reconstructive surgery
• Surgical accidents
• Hypercoagulable states
• Oral contraceptives

11. Arterial embolism
•Cardiac vegetation An abnormal growth of tissue around a valve, composed of blood platelets, bacteria, and a protein involved in clotting.
•Angiographic procedures
•Aortic atheroembolism

12. Venous thrombosis
• Hypercoagulable states induced, for example, by oral contraceptive or antithrombin III deficiency,
• intraperitoneal sepsis,
• the postoperative state,
• vascular invasive neoplasm (particularly hepatocellular carcinoma),
• cirrhosis,
• abdomina trauma.

13. Nonoclusive ischemia
• Cardiac failure
• Shock
• Dehydration
• Vasoconstrictive drugs

14. Miscellaneous
• Radiation injury
• Volvulus
• Stricture
• Internal & external herniation

15. Causes
• Ischemic bowel disease occurs when an artery that
supplies blood becomes blocked or narrowed.
There are several possible causes of ischemic bowel
disease, including:
• Blockage in the arteries due to a tumor or blood
clot
• Narrowing of the arteries supplying blood to the
bowel from atherosclerosis
• Obstruction in the colon (large intestine)

16. Risk Factors
• Advanced age
• Shock induced by conditions such as blood
stream infection and blood loss
• Recent heart attack
• Sustained abnormal heart beat
• Congestive heart failure
• Peripheral vascular disease
• Coronary artery bypass surgery or other vascular
surgeries

17. • Colon cancer
• Certain medications that cause arteries to narrow
• Diabetes
• Hemodialysis
• Sickle cell disease
• Dehydration
• Pregnancy

18. Pathophysiology
• Arterial sources v.s. venous sources:
proximately 9:1. Similarly, arterial occlusive
disease occurs more frequently than
nonocclusive disease approximately 9:1
• The SMA and IMA, and their branches, are
more frequently than the celiac artery.

19. Pathophysiology (a. source)
Acute:
1.atheromatous plaque with intimal calcifications
2.embolic from cardiac disease
3. abdominal aortic aneurysms with dissection into
SMA
4. hypoperfusion secondary to hypovolemic shock or
low-flow cardiac failure.

20. Pathophysiology (a. source)
Chronic :
1.atherosclerosis
2.fibromuscular dysplasia
3.vasculitis.
Both occlusive and nonocclusive subtypes can occur .

21. Pathophysiology (v. source)
• are less frequently.
• In these cases, bowel ischemia results from
decreased mesenteric outflow of
deoxygenated blood rather than from decreased
perfusion of oxygen-rich blood
• Mortality rates generally are low.
• SMV is involved more often than the IMV.

22. 3.Nonocclusive mesenteric ischemia
– more frequently in older patients than other
forms and often already in an ICU setting .
– Symptoms typically develop over several days,
and may have had a prodrome of malaise and
vague abdominal discomfort.
– When infarction occurs, increased pain associated
with vomiting,hypotensive and tachycardic, with
loose bloody stool.

23. 4.Mesenteric venous thrombosis
in a much younger patient population than other types .
– acute or subacute abdominal pain involvement of the
small intestine rather than the colon.
– The symptoms are frequently less dramatic. 27% have
symptoms for >30 d.
– Many patients have a history of the risk factors for
hypercoagulability. include oral contraceptive use, deep
vein thrombosis (DVT), liver disease, tumor, or portocaval
surgery.

24. Pathogenesis
Intestinal responses to ischemia occur in two
phases.
I. The initial hypoxic injury occurs at the onset
of vascular compromise. While some damage
occurs during this phase, the epithelial cells
lining the intestine are relatively resistant to
transient hypoxia.

25. II. The second phase, reperfusion injury, is initiated
by restoration of the blood supply and it is at this
time that the greatest damage occurs.
In severe cases this may trigger
multiorgan failure.
While the underlying mechanisms of reperfusion
injury are incompletely understood, they involve
free radical production, neutrophil infiltration, and
release of inflammatory mediators, such as
complement proteins and TNF.

26. • Activation of intracellular signaling
molecules and transcription factors,
including hypoxia-inducible factor 1 (HIF-1)
and NF-κB(nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that
controls the transcription of DNA) also contribute to intestinal
ischemia-reperfusion injury

27. • The severity of vascular compromise,
• the time frame during which it develops, and
• the vessels affected
are the major variables in
ischemic bowel disease.

28. • Two aspects of intestinal vascular anatomy also
contribute to the distribution of ischemic damage.
1. Intestinal segments at the end of
their respective arterial supplies
are particularly susceptible to
ischemia.
Tail enders

29. • These watershed zones include the
splenic flexure, where the superior
and inferior mesenteric arterial circulations
terminate, and, to a lesser extent,
• the sigmoid colon and rectum where
inferior mesenteric, pudendal, and iliac arterial
circulations end.

30. • Generalized hypotension or hypoxemia can
therefore cause localized injury, and ischemic
disease should be considered in the
differential diagnosis of focal colitis of the
splenic flexure or
• rectosigmoid colon.

31. 2. Intestinal capillaries run alongside the glands,
from crypt to surface.

32. •This allows oxygenated
blood to supply crypts but
leaves the surface epithelium
vulnerable to ischemic injury.
• This anatomy protects the crypts, which contain
the epithelial stem cells that are necessary to
repopulate the surface.

33. • Thus, surface epithelial atrophy,
or even necrosis and sloughing,
with normal or
hyperproliferative crypts
is a morphologic signature of ischemic
intestinal disease.

34. Morphology
Transmural Intestinal Infarction-
may involve a short or long segment, depending on
the particular vessel affected and the patency of
the anastomotic supply. Whether the occlusion is
arterial or venous, the infarction
always has a
dark red hemorrhagic appearance (Red
Infarction).

35. • The ischemic injury usually begins in the
mucosa and extends outwards;
within 18 to 24 hours.
• There is a thin, fibrinous exudate
over the serosa.

36. • With arterial occlusion the demarcation
from adjacent normal bowel is fairly sharply
defined, but
• with venous occlusion the margins are less
distinct.

37. • Affected foci may or may not be visible
from the serosal surface, because by
definition the ischemia does not affect the
entire thickness of the bowel.
• When the bowel is opened, hemorrhagic
edematous thickening of the mucosa,
sometimes with superficial ulcerations, is
seen.

38. EHNE
Histologic features are those of
acute injury:
Edema, hemorrhage, and outright necrosis of
the affected tissue layers.
Inflammation develops at the margins of the
lesions, and an inflammatory fibrin-containing
exudate (pseudomembrane), usually
secondary to bacterial superinfection, may
coat the affected mucosa.

39. • Alternatively, Chronic vascular insufficiency may
produce a
chronic inflammatory and ulcerative condition,
mimicking idiopathic inflammatory bowel disease.

40. •Lecture
12

41. Morphology –Transmural infarction
• Histologically, the changes are typical of ischemic
damage with
• marked edema,
• interstitial hemorrhage,
• necrosis and sloughing of the mucosa.
• Within 24 hours intestinal bacteria produce
outright gangrene and sometimes perforation of
the bowel.

42. Mural & mucosal infarctions-
are recognised by multifocal lesions
interspersed with spared areas.
Their location depends in part on
the extent of preexisting atherosclerotic narrowing of
the arterial supply;
lesions can be scattered over large regions of the
small or large intestines.
Patchy lesions
(Necrosis)

43. Symptoms
• Cramping and abdominal pain
• Bloody stools
• Frequent urge to defecate
• Diarrhea
• Nausea or vomiting
• Abdominal distension

44. Ischemia bowel
• acute or chronic.
• arterial or venous
• occlusive or nonocclusive.

45. Acute transmural infarction
typically presents with
sudden, severe abdominal pain
tenderness (more sudden with mesenteric embolism),
sometimes accompanied by
nausea,
vomiting,
bloody diarrhea, or
grossly melanotic stool.

46. Patients may progress to shock and vascular collapse within hours as a result of blood
loss. Peristaltic sounds diminish or disappear, and
muscular spasm creates
board-like
rigidity of the
abdominal wall.

47. Because these physical signs overlap with those of
other abdominal emergencies, including
acute appendicitis,
perforated ulcer, and
acute cholecystitis,
the diagnosis of intestinal necrosis may be
delayed or missed,
with disastrous consequences.

48. As the mucosal barrier breaks down, bacteria enter the circulation and
sepsiscan develop;
mortality may exceed 50%.
The overall progression of ischemic enteritis depends on the underlying
cause and severity of injury.

49. • The mortality rate with infarction of
the bowel approaches 90%, largely
because
the window of time between onset
of symptoms and perforation
caused by gangrene is so small.

50. Mucosal and mural infarctions
by themselves may not be fatal. However, these may progress to more extensive
infarction
if the vascular supply is not restored by correction of the
insult
or,
in chronic disease, by development of adequate
collateral supplies.

51. • The diagnosis of nonocclusive ischemic enteritis and
colitis can be particularly difficult because there may be a confusing array of
nonspecific abdominal symptoms, including
intermittent bloody diarrhea
and
•intestinal pseudo-obstruction.

52. ,
Chronic ischemia may masquerade as
inflammatory bowel disease, with episodes of
bloody diarrhea interspersed with periods of healing.

53. Diagnosis
• X-ray of abdomen
• CT Scan or MRI of the abdomen
• Colonoscopy—a procedure where a long
flexible tube is inserted through the rectum to
inspect the colon and rectum.
• Angiography—an x-ray test used to view the
arteries supplying the bowel

54. Differential
Appendicitis
Trauma
Pseudomembranous colitis Adenocarcinoma
Diverticulitis
Crohn Disease
Necrotizing Enterocolitis
Pneumatosis Intestinalis
Typhlitis
Ulcerative Colitis

55. Treatment
Supportive Care
• Bowel rest and intravenous fluids are given in mild
cases without significant progressed damage to the
bowel.
• Antibiotics
• Antibiotics are administered to minimize infection,
which can quickly complicate an ischemic bowel.
• Surgery
• In more severe cases, surgery is required to remove
the ischemic colon.

56. Complications
• Bowel necrosis (requiring bowel resection)
• Septic shock
• Death
• Patients in whom the diagnosis is missed until infarction
occurs have a mortality rate of 90%. Even with good
treatment, up to 50-80% of patients die.
• Survivors of extensive bowel resection face lifelong disability.

57. Prevention
• Stay well hydrated.
• Reduce your risk of cardiovascular disease
through regular exercise and a balanced diet
low in fat and calories.
• Consume plenty of fresh fruits, vegetables,
and fiber, which may reduce your risk of colon
cancer.

58. Major Causes of
Intestinal
Obstruction

59. Major Causes of Intestinal Obstruction
Mechanical Obstruction:
• Hernias
• Adhesions
• Intussuception
• Volvulus 80%

60. Intestinal obstruction. The four major causes of intestinal obstruction are (1)
herniation of a segment in the umbilical or inguinal regions, (2) adhesion between
loops of intestine, (3) volvulus, and (4) intussusception.

61. Other less frequent conditions
• Tumors & Infarction 10-15 %
• Inflammatory strictures
• Obstructive gall stones, fecaliths, foreign bodies
• Congenital Strictures, atresias
• Congenital bands
• Meconium in cystic fibrosis
• Imperforate anus