Ischemic Colitis



Ischemic Colitis

➢ Mesenteric Vascular Disease

• Superior Mesenteric Artery Embolism

Superior Mesenteric Artery Thrombosis

• Nonthrombotic Mesenteric Ischemia and Infarction

• Mesenteric Venous Occlusion

• Chronic Mesenteric Vascular Disease

• Ischemic Colitis

Vascular Anatomy

➢ The intestinal blood flow = 1500~1800 ml/min

--- variation in response to meals and exercise

➢ Three Main vessels

• Celiac Trunk

Splenic a.,

Common hepatic a.,

L’t gastric a.

--- Pancreaticoduodenal loop, Dorsal pancreatic a.

• SMA – Superior Mesenteric Artery

Inf. Pancreaticoduodenal a.

Mesenteric arteries to jejunum and ileum

Ileocolic a.

R’t colic a.

Middle colic a.

--- Meandering a.(communicating a., arc of Riolan, central anastomotic a.)

• IMA – Inferior Mesenteric Artery

L’t colic a.

Sigmoid a.

Superior rectal a.

--- Hypogastric A. ( rectal aa.

Pathophysiology of Intestinal Ischemia

Ischemia – inadequate perfusion from focal occlusion or a low-flow state

Thrombosis or embolism – 30 ~ 70 % of intestinal infarction

Inadequate perfusion – nonocclusive intestinal ischemia

e.q. : hypotension, spasm, intestinal distension

Early phase :

Volume loss and acidosis ( reversal of ischemic injury is possible

Later phase :

Bacteria invasion with endotoxin released, Septicemia, shock

( full-thickness irreversible injury

Systemic condition :

Intensive outpouring of protein and fluid through the injured villus

---- Loss of circulatory blood volume

( absorptive function of villus tip –injured; secretive function of crypt cell spared )

Intraluminal exudation ( loss of circulating volume and distension ( decrease in perfusion

Bowel edema and transudation of fluid into peritoneal cavity

( complicating the serious hypovolemia

Vasoactive substance

Myocardial depressant factor ( worsen decrease cardiac output

VIP ( vasoactive intestinal polypeptide )( vasodilator ( outpouring of intraluminal fluid

Histamine – released in ischemic reperfusion ( Shock

■ antagonist : Diamine oxidase

➢ Bacterial invasion

Occur >= 24 hours after ischemia

In 72 hours :

Anaerobic bacteria increase ( Bacteroides, Clostridial spp.)

Aerobic bacteria decrease

Portal venous bacteremia in 24 hours

( systemic bacteremia in 48 hours

( perforation ( gross contamination

➢ Oxygen free radicals ( -- occurred in reperfusion )

Source :: Peroxidation of lipid components of cellular membrane

Degradation of hyaluronic acid and collagen component of basement membrane

Hypoxia ( oxygen free radicals ( cytotoxic hydroxyl free radicals

↑(—)

Superoxide dismutase and catalase

( vascular permeability increase and mucosa membrane injury

( transcapillary fluid transudation and interstitial edema

Diagnostic study

WBC increase --- 12 % ~25 % WNL

Hct increase ( sludge and microvascular thrombosis

ABG ( metabolic acidosis may precede shock

Serum Phosphate increase ( precede irreversible ischemic injury

Amylase, LDH, GOT, CPK increase – but non-specific

Ischemic Colitis

Boley et al. ( 1963 )– a reversible component to colonic ischemia

Marston et al. ( 1966 )—three stages of ischemic colitis and the nature history

Age : 60 – 90 Y/O

Sex : Male > = Female

Etiology

Watershed phenomenon –

“Griffith’s point” – Splenic flexure – IMA and SMA junction

“Sudeck’s critical point” – Midportion of S-colon – IMA and hypogastric a.

➢ Recent Study of 1024 cases

R’t colon 8 %

T-colon 15 %

Splenic flexure 23 %

D-colon 27 %

S-colon 23 %

Rectum 4 %

The severity of ischemic colitis was influenced by

The duration of the decrease of blood flow

The adequacy of collateral circulation

The concentration of the colonic bacteria – when the mucosa barrier was comprised

Distension of the colon segment – decrease transmural blood flow

The predisposing factor

Underlying disease : artherosclerosis,

vasculitis,

collagen vascular disease,

CHF,

Polycythemia vera

Surgery : Aortic surgery with IMA ligation,

colonic surgery

Medication : digitalis,

Anti-HT agents,

diuretics,

oral contraceptives,

Catecholamines,

vasopressors

Hypotension or low-flow state: myocardial infarction,

sepsis,

trauma,

hypovolemia

Nature History

3 phases

Transient ischemic phase ---- 1/3 cases

Ischemic stricture –A late sequela of partial thickness injury

A gangrenous phase – 50 % cases

➢ Transient ischemic phase : reversible change confined to the mucosa and submucosa

Colonoscopy :: Mucosal edema

Congestion

Superficial ulceration

petechiae

Histology :: Mucosa superficial sloughing

Submucosal hemorrhage

X-ray finding : Thumbprinting – submucosal hemorrhage

Pseudotumor – distortion of bowel lumen by submucosal hemorrhage

➢ Ischemic stricture – partial thickness injury of mucosa and muscular layer ( fibrosis and narrowing of the lumen

Colonoscopy :: Fixed narrowing of lumen

Mucosa replaced by granulation tissue

Histology :: Marked fibrosis within the muscularis

Mucosa replaced by granulation tissue

Hemosiderin-laden macrophage are prevalent

X-ray finding : irreversible narrowing of the lumen with proximal colon maybe dilate

➢ Gangrenous ischemic colitis : Full-thickness necrosis and infarction

Gross : Dilated segment

Patchy or confluent gray-green or black discoloration

Histology : intense inflammation with transmural necrosis

X-ray finding : Should be AVOID

Clinical course : perforation, sepsis, and death

Diagnosis

Sudden onset abdominal pain

Bloody diarrhea

Fever

Abdominal distension

Previous – LGI or laparotomy

Present – colonoscopy and biopsy

Angiography is usually not helpful

Treatment

Consevative – if diagnosed early

OPD F/U (Liquid diet

Close observation

Antibiotics –possibly

Hospitalization :

bowel rest

NG decompression

IV fluid replacement – maybe TPN

Antibiotics –broad spectrum

Papaverine or Dextran ( to improve flow – but not proved

Surgical indication :

perforation

Sepsis

Fail to improve after conservative treatment

Stricture with obstruction or protracted bleeding or malignancy was suspected

Procedure :

Extended resection of nonviable colon

Prevent primary anastomosis – post OP progression of ischemia

Ischemic colitis and aortic surgery

➢ Ischemic colitis following aortic surgery is unique – Maybe a direct consequence of anatomic change of blood flow post IMA ligation

➢ Hagihara et al Ischemic colitis following abdominal aortic aneurysm resection – Clinically 1 % ~ 2%

Endoscopically 6.8 %

➢ Emergent repair of abdominal aortic aneurysm -- 60 % of patient has endoscopically ischemic colitis – maybe due to hypovolemia, shock, and no mechanical or antibiotic colon preparation

➢ Mortality of ischemic colitis following aortic surgery

-- 40 % ~ 65 %

-- Higher in case post emergent aortic surgery

➢ Etiology

Loss of blood flow from a patent IMA

Failure to resume hypogastric flow

Absence or injury of collateral circulation

Operative trauma of colon

Cholesterol emboli

Aortoiliac steal syndrome -- shunting of blood from colon

➢ Risk factor Prolonged crossclamp time

Rupture of the aneurysm

Hypotension

Arrhythmia

Ligation of a patent IMA

Treatment : Re-implaint of IMA – Depend on the Doppler ultrasound, fluorescein dye injection or IMA stump pressure

大腸直腸外科

葉 重 宏

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