Acute Mesenteric Ischemia (AMI)
rare but mortality 25-80% even in modern era
related to challenges & delay in diagnosis
anatomy & physiology review
SMA is primary small bowel supply (some collateral flow from celiac & IMA)
splanchnic circulation receives 20-35% of CO, depending on feeding state
70% of this circulation is directed to bowel mucosa & submucosa
splanchnic O2 extraction is low → requires 50% reduction before small bowel ischemia
studies show that mesenteric ischemia does not occur until MAP ≤ 45
bowel can compensate for up to 75% reduction in blood flow for up to 12h
intrinsic & extrinsic regulatory mechanism of mesenteric blood flow
intrinsic
hypoxic vasodilation
reactive hyperemia
pressure-flow autoregulation
myogenic factors (ie ↓perfusion w/reflexive vasoconstriction)
metabolic factors (ie O2 supply/demand imbalance, ↑K, acidosis)
extrinsic
mural (autonomics → alpha-adrenergic fibers → vasoconstriction → ↑splanchnic flow)
humural (ie norepinephrine, epinephrine, dobutamine, dopamine
pathogenesis: sustained bowel hypoperfusion → ischemic mucosa & submucosa injury
↑permeability/disruption → bacterial translocation
sloughing → diarrhea w/wo blood
infarction & necrosis → perforation → peritonitis & sepsis
+/- reperfusion injury → organ dysfunction s/p tx
etiology
Embolism of the SMA
classically reported to account for 40-50% of causes
majority 2/2 cardiac mural thrombus (uncommonly 2/2 coronary/cerebral angiography)
majority lodge in SMA 2/2 oblique angle from which it arises from aorta
50% lodge 3-6 cm distal to middle colic artery (ie 1st major branch of SMA)
typically less severe vs thrombosis (classically spares proximal jejunum and colon)
Thrombosis of the SMA
historically 25-30% of cases; modern cases series suggest now leading cause
virtually all occur 2/2 severe atherosclerotic disease (most commonly at origin of SMA)
slow progressive nature of atherosclerosis allows collateral flow development
typically more severe vs embolism (can extend duodenum to transverse colon)
Mesenteric Vein Thrombosis
least common, reported in up to 10% of cases
2/2 intra-abdominal pathology (ie malignancy, pancreatitis) or hypercoagulability
usually results in a more segmental ischemia, often involves PV or SMV or both
transition from viable/non-viable bowel is gradual
Non-Occlusive Mesenteric Ischemia (NOMI) aka low-flow state
accounts for 20% of cases
classically incl.
CKD pt on iHD who becomes hypotensive and develops diffuse abdominal pain
critically ill pts on multiple vasopressors
tends to affect watershed areas
SMA-IMA (Griffiths point or splenic flexure)
SRA-MRA (Sudeck point or rectosigmoid junction)
clinical
severe abd pain out of proportion to a soft abd exam
need to have a high index of suspicion
n/v w/diarrhea +/- blood in stools
33% present w/triad of abd pain, fever, hemoccult+ stool
arterial embolism: acute severe pain, hx AFib, PO intolerance
arterial thrombosis: post-prandial pain, unintentional wt loss
venous thrombosis: subacute pain, anorexia, hypovolemia
NOMI: critical illness, multiple pressors, abd distension, sepsis
workup
vitals may normal-to-deranged
severe hypovolemia can result 2/2 bowel edema
↑WBC, abnormal lytes, ↑amylase, lactic acidosis are non-specific
a normal lactate does not r/o AMI
obtain ECG w/troponins to r/o arrhythmia and recent MI
CT abdomen/pelvis w/contrast
may be non-diagnostic or show evidence of occlusion vs non-occlusion
be cautious: the following imaging may delay treatment
MRA obviates contrast but requires time and produces lower resolution images
risks of delaying correct diagnosis outweigh risks of contrast (get the CT)
plain films can show pneumoperitoneum or PVG but do not identify cause
duplex US is not usually useful in AMI 2/2 overlying bowel edema
TTE can delineate cardiac source of emboli but should not delay revascularization
when diagnosed and treated w/in 24h of sx onset, survival is still only 50%
drops sharply to < 30% w/delays in diagnosis
diagnosis: mesenteric CTA w/arterial and venous phase
arterial embolism: meniscus sign w/abrupt occlusion of SMA several centimeters from origin
arterial thrombosis: SMA occlusion at origin often w/enlarged collaterals
take note of calcifications on pre-contrast images esp. SMA os in the saggital plane
venous thrombosis: splenomegaly & ascites
other: abnormal bowel wall enhancement, intestinal dilation & thickening, pneumatosis intestinalis, portal venous gas, splenic or kidney infarction, free abdominal fluid, aortic dissection
therapy
early & aggressive resuscitation (fluids, lytes, etc.)
+/- vasopressors (only if needed)
broad spectrum abx if concern for bowel infarction
NGT (decompress bowel) & Foley (monitor UOP)
systemic heparinization
indications for emergent surgery
peritonitis
pneumoperitoneum
pneumatosis
HDUS
goals of emergent surgery
establish goals of care
reestablish blood flow to ischemic bowel
SMA embolus: embolectomy w/primary closure or patch angioplasty
SMA thrombosis: vein graft bypass (ex. retrograde iliac to distal SMA)
venous thrombosis & NOMI: supportive +/- IR systemic vs directed thrombolysis
resect all non-viable segments of bowel
preserve all potentially viable bowel (place temporary abd closure and go to ICU)
determining bowel viability (probably best for 2nd-look)
palpation of SMA pulse
anti-mesenteric Doppler signal
fluorescein injection f/b Wood's lamp exam
intentional enterotomy to assess for bleeding
evidence of peristalsis
indocyanine green (ICG) w/SPY portable handheld imager (SPY-PHI)
options for pts w/o emergent indications but w/significant occlusion
endovascular embolectomy
thrombolysis w/wo stenting
prognosis
peri-op mortality for revascularization ranges 40-90%
subset of pts who survive may develop short gut syndrome
Chronic Mesenteric Ischemia
TBD