Ischemic Colitis

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 SupplyCecum, Ascending & Proximal Transverse colon (Rt. 2/3) by:SMA and its branches: - Ileo-colic - Middle colic- Right colic

Arterial Blood SupplyDescending, 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 AREASAreas 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%):

reversiblenon-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 MedicationsThe 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 IschemiaMucosal infarction in which ischemic damage is confined to the mucosa

2. Partial thickness ischemiaMural infarction in which the injury extends from the mucosa into the muscularis mucosa

3. Full thickness infarctionTransmural infarction

• Transient Ischemia/ Partial ThicknessResult 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

LABSLabs will be Normal in mild casesSevere ischemia or necrosis may produce:- leukocytosis,

-metabolic acidosis,-or an elevated lactate.

ABDOMINAL X RAYAbdominal 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 ENEMAContrast 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' DIAGNOSINGISCHAEMIC COLITIS

SPLENIC FLEXURE SACCULATION AND STRICTURING AS SEQUELAE TOISCHAEMIC 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.

CTContrast 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 “LITTLEROSE” 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 colitideso ulcerative colitiso Crohn colitiso infective colitis: pseudomembranous, amebiasis,

schistosomiasiso 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 infarctionSurgical 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…