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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