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