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ISCHEMIC COLITIS
Dr. Ishfaq A. Shad
PROTOCOL
 DEFINATION
 ANATOMY
 CAUSES
 PATHOPHYSIOLOGY
 DIFFERENT PHASES
 CLINICAL PRESENTATION
 INVESTIGATIONS
 COMPLICATIONS
 DIFFERENTIAL DIAGNOSIS
 MANAGEMENT
 CONCLUSION
DEFINATION
 Ischaemic colitis refers to inflammation of the colon
secondary to vascular insufficiency and ischaemia. It is
sometimes considered under the same spectrum
of intestinal ischaemia. The severity and consequences
of the disease are highly variable.
 Ischemic colitis encompasses a number of clinical
entities, all with an end result of insufficient blood
supply to a segment or the entire colon.
 Ischemic colitis is the most common form of
gastrointestinal (GI) ischemia, accounting for 50 to
60% of all cases and occurring with an incidence of
4.5 to 44 cases per 100,000 person years.
 It accounts for 1 in 2000 hospital admissions. The
causes of ischemic colitis are numerous, but all
lead to diminished perfusion of the colon, which in
turn leads to mucosal injury or even full-thickness
necrosis.
ANATOMY
Arterial Blood
Supply
Cecum, Ascending
& Proximal
Transverse colon
(Rt. 2/3) by:
SMA and its
branches:
- Ileo-colic
- Middle colic
- Right colic
Arterial Blood
Supply
Descending,
Sigmoid, Distal
Transverse Colon
(Lt. 1/3) &
Rectum by:
IMA & its
branches
- Left colic
- Sigmoid
 The SMA and IMA communicate through the Marginal Artery
of ‘Drummond’, runs in the mesentery close to the bowel
along the splenic flexure.
 Points of communication between collateral arteries
are at higher risk for ischemia
 These points are:
 the splenic flexure
 the recto sigmoid junction
 However any segment of the colon may be
involved.
WATERSHED AREAS
Areas that are prone to Ischemia during
hypoperfusion & these areas lack in Anastomosis or
they have small amount of blood flow.
(1) the splenic flexure
(called as Griffitt’s Point)
between the SMA and IMA blood supply
(2) the distal sigmoid colon
(called as Sudek’s Point)
between the IMA and hypogastric artery supply
Limited collateral networks and are more
vulnerable to low flow states
Right Vs. Left
• The vasa recta are smaller and less
developed in the right colon
• These vessels are sensitive to
vasospasm
This explains the susceptibility of the
right colon to ischemia
PATHOPHYSIOLOGY
 Colonic blood supply
 The colon receives blood from both the superior and
inferior mesenteric arteries.
 The blood supply from these two major arteries overlap
with abundant collateral circulation.
 There are vascular “weak” points, at the borders of the
territory supplied by each of these arteries.
 These watershed areas are most vulnerable to ischemia
when blood flow decreases, as they have the fewest
vascular collaterals.
 The rectum receives blood from both the inferior
mesenteric artery and the internal iliac arteries.
 The rectum is rarely involved with colonic ischemia due
to this dual blood supply.
 Development of ischemia—
 Under ordinary conditions, the colon receives between
10% and 35% of the total cardiac output.
 If blood flow to the colon drops by more than about
50%, ischemia will develop.
 The arteries feeding the colon are very sensitive to
vasoconstrictors.
 As a result, during periods of low blood pressure, the
arteries feeding the colon clamp down vigorously.
 A similar process can result from vasoconstricting drugs
such as ergotamine, cocaine, or vasopressors.
 This vasoconstriction can result in non-occlusive
ischemic colitis.
Different pathological outcomes include :
 gangrenous (15-20%)
 non-gangrenous (80-85%):
 reversible
 non-reversible
(chronic colitis, stricture formation)
 The majority of patients (85%) develop non-gangrenous
ischemia, which is usually transient and resolves without
sequelae. Only a minority of these patients develop
long-term complications, which include persistent
segmental colitis and the development of a stricture.
Approximately 15% of patients with colonic ischemia
develop gangrene, the consequences of which are life-
threatening sepsis, bowel infarction, and death.
 Reversible colopathy
 Transient colitis
 Chronic colitis
 Stricture
 Gangrene
 Fulminant universal colitis
CAUSES
 arterial occlusion:
 arteriosclerosis
 vasculitides
 arterial emboli
 venous thrombosis:
 hyper coagulative states including malignancy and
OCP use
 primary mesenteric venous thrombosis
 low flow states:
 hypotension
 congestive heart failure
 cardiac arrhythmias
 others:
 sickle cell disease
 radiation therapy
Major vascular occlusion
 Mesenteric artery thrombosis
 Cholesterol emboli
 Colectomy with IMA ligation
 Aortic dissection
 Aortic reconstruction
 Mesenteric venous thrombosis
 Hypercoagulable state
 Lymphocytic phlebitis
 Portal hypertension
 Pancreatitis
Small vessel disease
 Diabetes
 Vasculitis
 Polyarteritis nodosa
 Lupus erythematosus
 Takayasu arteritis
 Wegener's granulomatosis
 Anticentromere antibodies
 Buerger's disease
 Antiphospholipid antibodies
 Amyloidosis
 Rheumatoid arthritis
 Radiation
Mechanical obstruction
 Strangulated hernia
 Colon cancer
 Adhesion
 Rectal prolapse
 Fecal impaction or pseudoobstruction
Shock
 Cardiac failure
 Hemodialysis
 Pancreatitis
 Anaphylaxis
Blood dyscrasia
 Hypercoagulable state
 Sickle cell disease
Iatrogenic
 Surgical
 Aortoiliac reconstruction
 Cardiopulmonary bypass
 Renal transplant
 Colonoscopy
 Barium enema
Drugs
 Digitalis
 Diuretics
 Cocaine
 Estrogens
 Danazol
 NSAIDs
 Tegaserod
 Vasoactive substances
 Paclitaxel and carboplatin
 Sumatriptan
 Simvastatin
Others
 Long distance running
 Dialysis
 Neurogenic
 Spontaneous in young adults
 Infections (CMV, E. coli O157:H7)
 Airplane flight
RISK FACTORS
 Suspect for Ischemic Colitis if:
 Older than 60
 Hemodialysis
 Hypertension
 Hypoalbuminemia
 Diabetes Mellitus
 Constipation-induced Medications
The presence 4 or more risk factors was 100% predictive
of Ischemic Colitis.
(Park CJ et al,2007)
CLINICAL PRESENTATION
SIGNS & SYMPTOMS
 Three progressive phases of Ischemic Colitis have been
described:
 A Hyperactive Phase occurs first in which the primary
symptoms are severe abdominal pain & the passage of
bloody stools. Many patients get better & do not progress
beyond this phase.
 A Paralytic Phase if ischemia continues. In this phase the
abdominal pain becomes more widespread, the belly
becomes more tender to the touch & the bowel motility
decreases resulting in abdominal bloating, no further bloody
stools & absent bowel sounds on exam.
 Finally, a Shock Phase can develop as fluids start to leak
through the damaged colon lining. This can result in shock &
metabolic acidosis with dehydration & low blood pressure,
rapid heart rate & confusion.
PHASES OF IC
• Regardless of the mechanism, the
disease follows the same course.
• Depending on the cause and severity,
the morphologic pattern can be
divided into 3 groups:
1. Transient Ischemia
Mucosal infarction in which ischemic damage is
confined to the mucosa
2. Partial thickness ischemia
Mural infarction in which the injury extends from
the mucosa into the muscularis mucosa
3. Full thickness infarction
Transmural infarction
• Transient Ischemia/ Partial Thickness
Result of hypoperfusion rather than occlusive
disease.
May involve any part of the gut and is usually
patchy and segmental.
• Full thickness
Result of thrombosis or embolism of SMA
More common in the small bowel, dependent on
the mesenteric blood supply.
Usually involves a long segment of bowel, tends
to occur in the 2 watershed territories.
INVESTIGATIONS
LABS
Labs will be Normal in mild cases
Severe ischemia or necrosis may
produce:
- leukocytosis,
-metabolic acidosis,
-or an elevated lactate.
ABDOMINAL X RAY
Abdominal radiographs are often normal, but signs
include:
 dilatation due to ileus
 'thumbprinting' due to mucosal
oedema/haemorrhage
 localised intramural gas (pneumatosis coli) if
necrotic
 free intraperitoneal gas if perforated
THE THUMBPRINTING OF THE DISTAL TRANSVERSE COLON IN ISCHEMIC COLITIS.
THE THUMBPRINTING OF THE SPLENIC FLEXURE AND THE ENTIRE DESCENDING COLON.
BARIUM ENEMA
Contrast enema is abnormal in 90% but is rarely
used for diagnostic purposes:
 segmental region of abnormality
 'thumbprinting' which is classically obliterated by air
insufflation
 spasm
 ulcerations 'serated mucosa'
 stricture from fibrosis as a late complication of
ischaemia
CLASSICAL SPLENIC FLEXURE 'THUMB-PRINTING' DIAGNOSING
ISCHAEMIC COLITIS
SPLENIC FLEXURE SACCULATION AND STRICTURING AS SEQUELAE TO
ISCHAEMIC COLITIS
DOUBLE-CONTRAST BARIUM ENEMA STUDY SHOWS A STRICTURE OF THE PROXIMAL DESCENDING
COLON SECONDARY TO ISCHEMIA.
ERECT RADIOGRAPH OBTAINED AFTER A DOUBLE-CONTRAST BARIUM ENEMA STUDY SHOWS A
STRICTURE AT THE SPLENIC FLEXURE.
CT
Contrast enhanced imaging is the modality of choice. Features
include:
 segmental region of abnormality
 symmetrical or lobulated thickening of bowel wall
 irregularly narrowed lumen
 submucosal oedema may produce low-density ring bordering
lumen (target sign)
 Irregular narrowing of the bowel lumen as a result of mucosal
edema (thumbprinting)
 intramural or portal venous gas
 mesenteric oedema
 superior mesenteric artery or vein thrombus/occlusion may be
demonstrated
 Nonspecific signs of bowel ischemia, including bowel
obstruction, mesenteric edema and ascites
LEFT SIDED COLONIC THICKENING
BEFORE REPERFUSION, COLONIC WALL APPEARS THINNED (PAPER-THIN WALL) AND HYPOTONIC
AFTER REPERFUSION, NOTE COLONIC WALL THICKENING (ARROW) AND PERICOLIC FLUID (STAR)
CONTRAST-ENHANCED CT IN PATIENTS WITH ACUTE OCCLUSIVE IC: HOMOGENEOUS LEFT COLONIC
INVOLVEMENT WITH DISAPPEARANCE OF THE LUMEN (ARROW) AND HYPERPERFUSION OF THE
MUCOSA IN CORONAL PLANE.
PATIENT WITH EMBOLIC IMA OCCLUSION IN ACUTE PHASE:
LEFT COLONIC WALL THICKENING (WHITE ARROW) WITH EVIDENCE OF “LITTLE
ROSE” SIGN OR TARGET ASPECT, PERICOLIC FLUID WAS ALSO PRESENT (CURVED ARROW)
AIR-CONTAINING, CYSTIC LUCENCIES ARE SEEN IN BOWEL WALL IN PROXIMAL DESCENDING
COLON (WHITE CIRCLE) AND IN THE WALL OF
THE LARGE BOWEL IN THE LOWER ABDOMEN (BLACK ARROWS).
PNEUMATOSIS INTESTINALIS ( INTRAMURAL GAS LIMITED TO THE COLONIC WALL)
MRI
 Sensitivity of MRI in the detection of bowel
ischemia is comparable to that of CT
 MRI may be useful in depicting bowel-wall changes
and in demonstrating mesenteric vascular
abnormalities.
 As with CT, the additional use of contrast
enhancement allows an assessment of the dynamic
changes in the bowel wall.
ULTRASONOGRAPHY
 Bowel gas frequently prevents the visualization of
colonic changes, which are usually most marked
around the splenic flexure.
 The bowel wall becomes thickened, and nodular
and intramural hemorrhage and edema give rise to
areas of reduced echogenicity.
 Echogenic areas may be seen in the bowel wall;
these may reflect either areas of infarction infiltrate
or clot.
MARKED THICKENING OF LEFT COLON
SEGMENTAL COLITIS INVOLVING SPLENIC FLEXURE, DESCENDING & SIGMOID COLONS (S).
TRANSVERSE SONOGRAM SHOWS THICKENING OF SIGMOID COLON WALL, WITH BARELY VISIBLE
COLOR DOPPLER FLOW (SHOWN HERE IN BLACK-AND-WHITE, ARROW)
AIR IN INTRAHEPATIC BRANCHES OF RIGHT PORTAL VEIN (ARROWS)
COLOR DOPPLER USG
 Color flow Doppler sonography is effective in
demonstrating flow disturbances associated with
tortuosity and stenosis at the origin of the celiac
axis.
NONSTRATIFIED THICKENING OF BOWEL WALL OF DESCENDING AND SIGMOID COLONS (S) AND ALTERED PERICOLIC
FAT (WHITE ARROWS). BARELY VISIBLE COLOR DOPPLER FLOW (ONLY ONE COLOR PIXEL) IS SEEN (BLACK ARROW).
ALSO NOTE VASCULAR ENGORGEMENT (ARROWHEADS).
ANGIOGRAPHY
 Angiography has a limited role in the diagnosis of
colonic ischemia, in most cases colonic blood flow
has already returned to normal by the time of
symptom onset.
 However, angiography may be indicated if the
clinical examination and other studies can not
exclude small bowel ischemia due to acute
proximal mesentric thrombus or embolus
 Can show mesenteric artery occlusion if present.
INFERIOR MESENTERIC ANGIOGRAM SHOWS A STENOSIS OF MORE THAN 50% AT THE ORIGIN OF
THE LEFT COLIC ARTERY ASSOCIATED WITH A POSTSTENOTIC DILATATION
NUCLEAR MEDICINE
 Increased uptake of Tc99m (V) DMSA (pentavalent
techenetium-99m dimercaptosuccinic acid) tracer in
the ischaemic bowel may be present but is
unreliable.
COLONOSCOPY
 The procedure of choice if the diagnosis remains
unclear
 Findings at colonoscopy depend on the stage and
severity of ischemia.
- Early stages of ischemia, petechial hemorrhages
are interspersed with areas of pale, edematous
mucosa.
- Later, segmental erythema, +/-ulcerations and
bleeding
 Colonoscopy is preferable to contrast enemas since it is
more sensitive in detecting mucosal lesions, permits
biopsies to be obtained, and does not interfere with
subsequent angiography.
COMPLICATIONS
Ischemic colitis usually gets better on its own
within two to three days. In more-severe cases,
complications can include:
 Tissue death (gangrene) resulting from
diminished blood flow
 Hole (perforation) in intestine or persistent
bleeding
 Bowel inflammation (segmented ulcerating
colitis)
 Bowel obstruction (ischemic stricture)
DIFFERENTIAL DIAGNOSIS
 Imaging differential considerations include:
 other colitides
o ulcerative colitis
o Crohn colitis
o infective colitis: pseudomembranous, amebiasis,
schistosomiasis
o radiation colitis
 intramural haemorrhage
 diverticulitis
 lymphoma or carcinoma
 The features considered atypical in
inflammatory bowel diseases , such as
1. segmental distribution of the disease,
infrequent rectal involvement,
2. high rate of spontaneous recovery,
low rate of recurrence,
3. lack of adequate response to usual inflammatory
bowel disease therapy,
4. frequent progression to fibrotic stenosis with
delayed obstruction
 The features above are now recognized as
characteristic of colonic ischemia.
CLINICALLY
Ulcerative colitis
 Bloody diarrhea
Crohn’s colitis
 Perianal lesions common; frank bleeding less
frequent than in ulcerative colitis
Ischemic Colitis
 Older age groups; vascular disease; sudden
onset, often painful
RADIOLOGICALLY
Ulcerative colitis
 Extends proximally from rectum; fine mucosal
ulceration
Crohn’s Colitis
 Segmental disease; rectal sparing; strictures,
fissures, ulcers, fistulas; small bowel
involvement
Ischemic Colitis
 Splenic flexure; “thumb printing”; rectal
involvement rare
MANAGEMENT
 Treatment of the patient is dictated by the
severity of the ischemia .
1. Transient Ischemia
 Treated symptomatically
 Observation with :
 Bowel rest, IVF, O2 and optomise cardiac function
2. Partial thickness ischemia
 Close observation, IVF, broad-spectrum antibiotics
 If stricture develops and is symptomatic, resection
may be required.
3. Full thickness infarction
Surgical resection
Full thickness/Gangrenous infarction
• Approximately 20% of patients with IC will
require surgery because of peritonitis or
clinical deterioration despite conservative
management
• Emergency resection of non viable bowel is
required and colostomy is usually done.
CONCLUSION
 Always consider the diagnosis of ischemic colitis
whenever contemplating the diagnosis of
inflammatory bowel disease in the elderly.
 Thumbprinting of the colon on plain abdominal
radiographs suggests ischemic colitis.
 CT with oral & IV contrast is the imaging modality of
choice to assess distribution & phase of Colitis
 Finding on CT or MRI (e.g., bowel wall thickening,
edema, thumbprinting, pericolonic fat stranding) are
suggestive of IC, but not specific for diagnosis
 CT (MRI) findings of colonic pneumatosis & porto-
mesentric venous gas are highly suggestive of
transmural colonic infarction, but not dignostic
 Common findings (good prognosis) are non-specific
& more specific findings (bad prognosis) are
Uncommon
 Evaluation is by CT & Colonoscopy not
Angiography
 CT scan is the initial screening test; may help determine
prognosis
 Colonoscopy is the test of choice for confirming
diagnosis; may help determine prognosis
 Antibiotics for moderate to severe Ischemic Colitis
 Surgical consultation is warranted in all cases of
suspected Ischemic Colitis.
THANKS…

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Ischemic Colitis

  • 2. PROTOCOL  DEFINATION  ANATOMY  CAUSES  PATHOPHYSIOLOGY  DIFFERENT PHASES  CLINICAL PRESENTATION  INVESTIGATIONS  COMPLICATIONS  DIFFERENTIAL DIAGNOSIS  MANAGEMENT  CONCLUSION
  • 4.  Ischaemic colitis refers to inflammation of the colon secondary to vascular insufficiency and ischaemia. It is sometimes considered under the same spectrum of intestinal ischaemia. The severity and consequences of the disease are highly variable.  Ischemic colitis encompasses a number of clinical entities, all with an end result of insufficient blood supply to a segment or the entire colon.
  • 5.  Ischemic colitis is the most common form of gastrointestinal (GI) ischemia, accounting for 50 to 60% of all cases and occurring with an incidence of 4.5 to 44 cases per 100,000 person years.  It accounts for 1 in 2000 hospital admissions. The causes of ischemic colitis are numerous, but all lead to diminished perfusion of the colon, which in turn leads to mucosal injury or even full-thickness necrosis.
  • 7. Arterial Blood Supply Cecum, Ascending & Proximal Transverse colon (Rt. 2/3) by: SMA and its branches: - Ileo-colic - Middle colic - Right colic
  • 8. Arterial Blood Supply Descending, Sigmoid, Distal Transverse Colon (Lt. 1/3) & Rectum by: IMA & its branches - Left colic - Sigmoid
  • 9.  The SMA and IMA communicate through the Marginal Artery of ‘Drummond’, runs in the mesentery close to the bowel along the splenic flexure.  Points of communication between collateral arteries are at higher risk for ischemia  These points are:  the splenic flexure  the recto sigmoid junction  However any segment of the colon may be involved.
  • 10. WATERSHED AREAS Areas that are prone to Ischemia during hypoperfusion & these areas lack in Anastomosis or they have small amount of blood flow. (1) the splenic flexure (called as Griffitt’s Point) between the SMA and IMA blood supply (2) the distal sigmoid colon (called as Sudek’s Point) between the IMA and hypogastric artery supply Limited collateral networks and are more vulnerable to low flow states
  • 11.
  • 12. Right Vs. Left • The vasa recta are smaller and less developed in the right colon • These vessels are sensitive to vasospasm This explains the susceptibility of the right colon to ischemia
  • 14.  Colonic blood supply  The colon receives blood from both the superior and inferior mesenteric arteries.  The blood supply from these two major arteries overlap with abundant collateral circulation.  There are vascular “weak” points, at the borders of the territory supplied by each of these arteries.  These watershed areas are most vulnerable to ischemia when blood flow decreases, as they have the fewest vascular collaterals.  The rectum receives blood from both the inferior mesenteric artery and the internal iliac arteries.  The rectum is rarely involved with colonic ischemia due to this dual blood supply.
  • 15.  Development of ischemia—  Under ordinary conditions, the colon receives between 10% and 35% of the total cardiac output.  If blood flow to the colon drops by more than about 50%, ischemia will develop.  The arteries feeding the colon are very sensitive to vasoconstrictors.  As a result, during periods of low blood pressure, the arteries feeding the colon clamp down vigorously.  A similar process can result from vasoconstricting drugs such as ergotamine, cocaine, or vasopressors.  This vasoconstriction can result in non-occlusive ischemic colitis.
  • 16. Different pathological outcomes include :  gangrenous (15-20%)  non-gangrenous (80-85%):  reversible  non-reversible (chronic colitis, stricture formation)
  • 17.  The majority of patients (85%) develop non-gangrenous ischemia, which is usually transient and resolves without sequelae. Only a minority of these patients develop long-term complications, which include persistent segmental colitis and the development of a stricture. Approximately 15% of patients with colonic ischemia develop gangrene, the consequences of which are life- threatening sepsis, bowel infarction, and death.  Reversible colopathy  Transient colitis  Chronic colitis  Stricture  Gangrene  Fulminant universal colitis
  • 19.  arterial occlusion:  arteriosclerosis  vasculitides  arterial emboli  venous thrombosis:  hyper coagulative states including malignancy and OCP use  primary mesenteric venous thrombosis  low flow states:  hypotension  congestive heart failure  cardiac arrhythmias  others:  sickle cell disease  radiation therapy
  • 20. Major vascular occlusion  Mesenteric artery thrombosis  Cholesterol emboli  Colectomy with IMA ligation  Aortic dissection  Aortic reconstruction  Mesenteric venous thrombosis  Hypercoagulable state  Lymphocytic phlebitis  Portal hypertension  Pancreatitis
  • 21. Small vessel disease  Diabetes  Vasculitis  Polyarteritis nodosa  Lupus erythematosus  Takayasu arteritis  Wegener's granulomatosis  Anticentromere antibodies  Buerger's disease  Antiphospholipid antibodies  Amyloidosis  Rheumatoid arthritis  Radiation
  • 22. Mechanical obstruction  Strangulated hernia  Colon cancer  Adhesion  Rectal prolapse  Fecal impaction or pseudoobstruction Shock  Cardiac failure  Hemodialysis  Pancreatitis  Anaphylaxis
  • 23. Blood dyscrasia  Hypercoagulable state  Sickle cell disease Iatrogenic  Surgical  Aortoiliac reconstruction  Cardiopulmonary bypass  Renal transplant  Colonoscopy  Barium enema
  • 24. Drugs  Digitalis  Diuretics  Cocaine  Estrogens  Danazol  NSAIDs  Tegaserod  Vasoactive substances  Paclitaxel and carboplatin  Sumatriptan  Simvastatin
  • 25. Others  Long distance running  Dialysis  Neurogenic  Spontaneous in young adults  Infections (CMV, E. coli O157:H7)  Airplane flight
  • 26. RISK FACTORS  Suspect for Ischemic Colitis if:  Older than 60  Hemodialysis  Hypertension  Hypoalbuminemia  Diabetes Mellitus  Constipation-induced Medications The presence 4 or more risk factors was 100% predictive of Ischemic Colitis. (Park CJ et al,2007)
  • 28. SIGNS & SYMPTOMS  Three progressive phases of Ischemic Colitis have been described:  A Hyperactive Phase occurs first in which the primary symptoms are severe abdominal pain & the passage of bloody stools. Many patients get better & do not progress beyond this phase.  A Paralytic Phase if ischemia continues. In this phase the abdominal pain becomes more widespread, the belly becomes more tender to the touch & the bowel motility decreases resulting in abdominal bloating, no further bloody stools & absent bowel sounds on exam.  Finally, a Shock Phase can develop as fluids start to leak through the damaged colon lining. This can result in shock & metabolic acidosis with dehydration & low blood pressure, rapid heart rate & confusion.
  • 30. • Regardless of the mechanism, the disease follows the same course. • Depending on the cause and severity, the morphologic pattern can be divided into 3 groups:
  • 31. 1. Transient Ischemia Mucosal infarction in which ischemic damage is confined to the mucosa 2. Partial thickness ischemia Mural infarction in which the injury extends from the mucosa into the muscularis mucosa 3. Full thickness infarction Transmural infarction
  • 32. • Transient Ischemia/ Partial Thickness Result of hypoperfusion rather than occlusive disease. May involve any part of the gut and is usually patchy and segmental. • Full thickness Result of thrombosis or embolism of SMA More common in the small bowel, dependent on the mesenteric blood supply. Usually involves a long segment of bowel, tends to occur in the 2 watershed territories.
  • 34. LABS Labs will be Normal in mild cases Severe ischemia or necrosis may produce: - leukocytosis, -metabolic acidosis, -or an elevated lactate.
  • 35. ABDOMINAL X RAY Abdominal radiographs are often normal, but signs include:  dilatation due to ileus  'thumbprinting' due to mucosal oedema/haemorrhage  localised intramural gas (pneumatosis coli) if necrotic  free intraperitoneal gas if perforated
  • 36. THE THUMBPRINTING OF THE DISTAL TRANSVERSE COLON IN ISCHEMIC COLITIS.
  • 37. THE THUMBPRINTING OF THE SPLENIC FLEXURE AND THE ENTIRE DESCENDING COLON.
  • 38. BARIUM ENEMA Contrast enema is abnormal in 90% but is rarely used for diagnostic purposes:  segmental region of abnormality  'thumbprinting' which is classically obliterated by air insufflation  spasm  ulcerations 'serated mucosa'  stricture from fibrosis as a late complication of ischaemia
  • 39.
  • 40.
  • 41. CLASSICAL SPLENIC FLEXURE 'THUMB-PRINTING' DIAGNOSING ISCHAEMIC COLITIS
  • 42. SPLENIC FLEXURE SACCULATION AND STRICTURING AS SEQUELAE TO ISCHAEMIC COLITIS
  • 43. DOUBLE-CONTRAST BARIUM ENEMA STUDY SHOWS A STRICTURE OF THE PROXIMAL DESCENDING COLON SECONDARY TO ISCHEMIA.
  • 44. ERECT RADIOGRAPH OBTAINED AFTER A DOUBLE-CONTRAST BARIUM ENEMA STUDY SHOWS A STRICTURE AT THE SPLENIC FLEXURE.
  • 45. CT Contrast enhanced imaging is the modality of choice. Features include:  segmental region of abnormality  symmetrical or lobulated thickening of bowel wall  irregularly narrowed lumen  submucosal oedema may produce low-density ring bordering lumen (target sign)  Irregular narrowing of the bowel lumen as a result of mucosal edema (thumbprinting)  intramural or portal venous gas  mesenteric oedema  superior mesenteric artery or vein thrombus/occlusion may be demonstrated  Nonspecific signs of bowel ischemia, including bowel obstruction, mesenteric edema and ascites
  • 46. LEFT SIDED COLONIC THICKENING
  • 47. BEFORE REPERFUSION, COLONIC WALL APPEARS THINNED (PAPER-THIN WALL) AND HYPOTONIC
  • 48. AFTER REPERFUSION, NOTE COLONIC WALL THICKENING (ARROW) AND PERICOLIC FLUID (STAR)
  • 49. CONTRAST-ENHANCED CT IN PATIENTS WITH ACUTE OCCLUSIVE IC: HOMOGENEOUS LEFT COLONIC INVOLVEMENT WITH DISAPPEARANCE OF THE LUMEN (ARROW) AND HYPERPERFUSION OF THE MUCOSA IN CORONAL PLANE.
  • 50. PATIENT WITH EMBOLIC IMA OCCLUSION IN ACUTE PHASE: LEFT COLONIC WALL THICKENING (WHITE ARROW) WITH EVIDENCE OF “LITTLE ROSE” SIGN OR TARGET ASPECT, PERICOLIC FLUID WAS ALSO PRESENT (CURVED ARROW)
  • 51. AIR-CONTAINING, CYSTIC LUCENCIES ARE SEEN IN BOWEL WALL IN PROXIMAL DESCENDING COLON (WHITE CIRCLE) AND IN THE WALL OF THE LARGE BOWEL IN THE LOWER ABDOMEN (BLACK ARROWS).
  • 52. PNEUMATOSIS INTESTINALIS ( INTRAMURAL GAS LIMITED TO THE COLONIC WALL)
  • 53. MRI  Sensitivity of MRI in the detection of bowel ischemia is comparable to that of CT  MRI may be useful in depicting bowel-wall changes and in demonstrating mesenteric vascular abnormalities.  As with CT, the additional use of contrast enhancement allows an assessment of the dynamic changes in the bowel wall.
  • 54. ULTRASONOGRAPHY  Bowel gas frequently prevents the visualization of colonic changes, which are usually most marked around the splenic flexure.  The bowel wall becomes thickened, and nodular and intramural hemorrhage and edema give rise to areas of reduced echogenicity.  Echogenic areas may be seen in the bowel wall; these may reflect either areas of infarction infiltrate or clot.
  • 55. MARKED THICKENING OF LEFT COLON
  • 56. SEGMENTAL COLITIS INVOLVING SPLENIC FLEXURE, DESCENDING & SIGMOID COLONS (S). TRANSVERSE SONOGRAM SHOWS THICKENING OF SIGMOID COLON WALL, WITH BARELY VISIBLE COLOR DOPPLER FLOW (SHOWN HERE IN BLACK-AND-WHITE, ARROW)
  • 57. AIR IN INTRAHEPATIC BRANCHES OF RIGHT PORTAL VEIN (ARROWS)
  • 58. COLOR DOPPLER USG  Color flow Doppler sonography is effective in demonstrating flow disturbances associated with tortuosity and stenosis at the origin of the celiac axis.
  • 59. NONSTRATIFIED THICKENING OF BOWEL WALL OF DESCENDING AND SIGMOID COLONS (S) AND ALTERED PERICOLIC FAT (WHITE ARROWS). BARELY VISIBLE COLOR DOPPLER FLOW (ONLY ONE COLOR PIXEL) IS SEEN (BLACK ARROW). ALSO NOTE VASCULAR ENGORGEMENT (ARROWHEADS).
  • 60. ANGIOGRAPHY  Angiography has a limited role in the diagnosis of colonic ischemia, in most cases colonic blood flow has already returned to normal by the time of symptom onset.  However, angiography may be indicated if the clinical examination and other studies can not exclude small bowel ischemia due to acute proximal mesentric thrombus or embolus  Can show mesenteric artery occlusion if present.
  • 61.
  • 62.
  • 63.
  • 64.
  • 65.
  • 66. INFERIOR MESENTERIC ANGIOGRAM SHOWS A STENOSIS OF MORE THAN 50% AT THE ORIGIN OF THE LEFT COLIC ARTERY ASSOCIATED WITH A POSTSTENOTIC DILATATION
  • 67. NUCLEAR MEDICINE  Increased uptake of Tc99m (V) DMSA (pentavalent techenetium-99m dimercaptosuccinic acid) tracer in the ischaemic bowel may be present but is unreliable.
  • 68. COLONOSCOPY  The procedure of choice if the diagnosis remains unclear  Findings at colonoscopy depend on the stage and severity of ischemia. - Early stages of ischemia, petechial hemorrhages are interspersed with areas of pale, edematous mucosa. - Later, segmental erythema, +/-ulcerations and bleeding  Colonoscopy is preferable to contrast enemas since it is more sensitive in detecting mucosal lesions, permits biopsies to be obtained, and does not interfere with subsequent angiography.
  • 70. Ischemic colitis usually gets better on its own within two to three days. In more-severe cases, complications can include:  Tissue death (gangrene) resulting from diminished blood flow  Hole (perforation) in intestine or persistent bleeding  Bowel inflammation (segmented ulcerating colitis)  Bowel obstruction (ischemic stricture)
  • 72.  Imaging differential considerations include:  other colitides o ulcerative colitis o Crohn colitis o infective colitis: pseudomembranous, amebiasis, schistosomiasis o radiation colitis  intramural haemorrhage  diverticulitis  lymphoma or carcinoma
  • 73.  The features considered atypical in inflammatory bowel diseases , such as 1. segmental distribution of the disease, infrequent rectal involvement, 2. high rate of spontaneous recovery, low rate of recurrence, 3. lack of adequate response to usual inflammatory bowel disease therapy, 4. frequent progression to fibrotic stenosis with delayed obstruction  The features above are now recognized as characteristic of colonic ischemia.
  • 74. CLINICALLY Ulcerative colitis  Bloody diarrhea Crohn’s colitis  Perianal lesions common; frank bleeding less frequent than in ulcerative colitis Ischemic Colitis  Older age groups; vascular disease; sudden onset, often painful
  • 75. RADIOLOGICALLY Ulcerative colitis  Extends proximally from rectum; fine mucosal ulceration Crohn’s Colitis  Segmental disease; rectal sparing; strictures, fissures, ulcers, fistulas; small bowel involvement Ischemic Colitis  Splenic flexure; “thumb printing”; rectal involvement rare
  • 77.  Treatment of the patient is dictated by the severity of the ischemia .
  • 78. 1. Transient Ischemia  Treated symptomatically  Observation with :  Bowel rest, IVF, O2 and optomise cardiac function 2. Partial thickness ischemia  Close observation, IVF, broad-spectrum antibiotics  If stricture develops and is symptomatic, resection may be required. 3. Full thickness infarction Surgical resection
  • 79. Full thickness/Gangrenous infarction • Approximately 20% of patients with IC will require surgery because of peritonitis or clinical deterioration despite conservative management • Emergency resection of non viable bowel is required and colostomy is usually done.
  • 81.  Always consider the diagnosis of ischemic colitis whenever contemplating the diagnosis of inflammatory bowel disease in the elderly.  Thumbprinting of the colon on plain abdominal radiographs suggests ischemic colitis.  CT with oral & IV contrast is the imaging modality of choice to assess distribution & phase of Colitis
  • 82.  Finding on CT or MRI (e.g., bowel wall thickening, edema, thumbprinting, pericolonic fat stranding) are suggestive of IC, but not specific for diagnosis  CT (MRI) findings of colonic pneumatosis & porto- mesentric venous gas are highly suggestive of transmural colonic infarction, but not dignostic  Common findings (good prognosis) are non-specific & more specific findings (bad prognosis) are Uncommon
  • 83.  Evaluation is by CT & Colonoscopy not Angiography  CT scan is the initial screening test; may help determine prognosis  Colonoscopy is the test of choice for confirming diagnosis; may help determine prognosis  Antibiotics for moderate to severe Ischemic Colitis  Surgical consultation is warranted in all cases of suspected Ischemic Colitis.