Page 1500 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 109: Mesenteric Ischemia 1039

SYSTEMIC RESPONSE TO MESENTERIC ischemia is considered. Acute mesenteric ischemia may present on
REVASCULARISATION a background of chronic intestinal angina or de novo in a previously
unsuspected individual with symptoms ranging from subtle signs of
On reperfusion of the acutely ischemic intestine, local injury can induce intra-abdominal sepsis to the dramatic acute abdomen.
a systemic response as metabolic byproducts of the ischemic process
(lactate, H , K , oxygen reactive species, arachidonic acid derivatives, ■ ACUTE EMBOLIC ARTERIAL OBSTRUCTION
+
+
cytokines, possibly endotoxin, and activated leukocytes) are flushed into Acute embolic obstruction of the SMA is characterized by acute onset
the portal and systemic circulation. A systemic inflammatory response
syndrome (SIRS) is initiated, triggering the complement and coagula- of severe central abdominal pain, often associated with nausea, vomit-
ing, and even diarrhea or a bowel movement. Pain often is described
tion cascades, elaborating cytokines, and provoking widespread endo-
thelial dysfunction and vital organ injury. Acute lung injury (ALI) is the as out of proportion to objective findings and is poorly localized until
advanced signs of peritonitis ensue. The patient often adopts a chin-
most common manifestation of the systemic inflammatory response to
intestinal reperfusion. to-knees body habitus, initially restless but later lying quietly once
peritonitis develops. In the early stages, abdominal examination may be
Though surviving this initial phase of acute gut-derived inflamma-
tion, the reperfused but injured intestine can continue to be detrimental truly unremarkable, perhaps with some diffuse tenderness but without
localized peritonitis. Development of an ileus or peritoneal findings is a
to the host. The gastrointestinal tract normally is inhabited by a large
collection of gram-negative bacteria. Gut-mucosal barrier disruption after grave sign suggestive of mesenteric infarction. Bloody diarrhea is a late
sign associated with mucosal disruption. Hypotension is common, but
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ischemia-reperfusion injury allows translocation of these bacteria. 16,17
The vast hepatic sinusoid network, lined with fixed-tissue macrophages sustained hypotension in the early stages is more likely due to a cardiac
than an intestinal cause. Embolic sources, such as arrhythmia (atrial
(Kupffer cells), is strategically located to interact with gut-derived
endotoxin and contribute to multiple-organ-system failure (MOSF). fibrillation), acute myocardial infarction, dilated cardiomyopathy, or a
recently instrumented aorta, should be sought.
Noncardiogenic pulmonary edema (ALI) is well recognized after intes-
tinal ischemia reperfusion injury. 14,18 Postoperative, renal, and hepatic ■
dysfunctions also are common. ACUTE THROMBOTIC ARTERIAL OCCLUSION
Thrombotic occlusion occurs often in the setting of chronic low-grade
INTESTINAL ISCHEMIA RISK FACTORS symptoms of chronic mesenteric ischemia. A history of weight loss,
intestinal angina, or altered bowel habit should be sought. The presence
A number of factors influence the development of and survival from of chronically developed collaterals may protect against distal ischemia,
acute mesenteric ischemia. Factors predisposing to occlusive mesen- making the presentation subtle and gradual, with only vague abdominal
teric ischemia include hypertension, tobacco use, family history of pain and altered bowel habit initially. However, preexisting atherosclerotic
cardiovascular disease, peripheral vascular disease, coronary artery disease in the other major mesenteric trunks will predispose to acute-on-
disease, diabetes, congestive heart failure, prior myocardial infarction, chronic thrombosis of the remaining trunk, critically restricting flow to
cerebrovascular disease, hypercholesterolemia, and atrial fibrillation. 19,20 the entire mesenteric bed and leading to massive mesenteric infarction.
Nonocclusive mesenteric ischemia results from splanchnic vasocon-
striction in response to systemic factors and is associated with acute ■ NONOCCLUSIVE MESENTERIC ISCHEMIA
cardiac dysfunction (myocardial infarction, arrhythmia, left ventricular There is increasing awareness of nonocclusive mesenteric ischemia
dysfunction), hypovolemia, and pharmacotherapy. Digitalis is an
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additional risk factor for developing NOMI. It induces vasoconstric- (NOMI). Any systemic hypoperfusion state can threaten the mesenteric
territory. Systemic hypoperfusion with local vasoconstriction results in
tion and thus an increased resistance in peripheral splanchnic vessels.
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Alkaloids constitute another substance group causing smooth muscle severely reduced mesenteric perfusion. Mesenteric vasoconstriction may
be precipitated by a variety of shock states, namely cardiogenic, septic,
contraction of the arteriolar wall. Ergotamine is one of the most potent 23
vasoconstrictors in this group, which plays an important pathogenic role neurogenic, hypovolemic, and even anaphylaxis. Furthermore, drugs
commonly used to treat acute cardiac dysfunction (digoxin, β-blockers)
in NOMI. 60,61 A combination of glycosides and diuretics is frequently
administered to patients with congestive heart failure. The increased and those employed to support the failing circulation (catecholamines,
vasopressin) may exacerbate mesenteric vasoconstriction. Therefore,
renal blood flow caused by furosemide leads to a diminished mesenteric
perfusion. This is probably due to the furosemide-related activation of NOMI should be considered early in any hypotensive patient with
suggestive findings. Clinical signs are often vague, with new or persis-
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the renin–angiotensin–aldosterone system with subsequently increased
levels of angiotensin II. 62,63 Other causes of mesenteric vasospasm are tent ileus, failure of intestinal feeding, abdominal distention, or sepsis of
unknown source. Rectal mucus, melena, or frank blood are nonspecific
various forms of shock, septicemia, dehydration, and hypotension
following dialysis and heart surgery or major abdominal surgery. The but may point to bowel ischemia. There may be a role for gastrointestinal
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balloon tonometry in identifying patients with or at risk of developing
frequent concomitance of pancreatitis in NOMI is explained by
the proximity of the superior mesenteric artery (SMA) and the celiac NOMI. Recreational drugs (eg, cocaine) have been reported recently to
cause acute NOMI, and a history should be sought if suspicion arises.
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plexus to the pancreas. The inflammation of the pancreas may induce a
Factors predictive of mortality secondary to intestinal ischemia ■
vasoconstrictive response in the superior mesenteric artery. 62 MESENTERIC VENOUS THROMBOSIS
include advanced age, generally poor health, diagnostic delay, and non- Mesenteric vein thrombosis most often results in a delayed presentation,
occlusive mesenteric ischemia. Most patients with asymptomatic high- often preceded by several weeks of intermittent abdominal pain and
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grade stenosis or occlusions of all three mesenteric trunks will develop altered bowel habit, but it also can cause acute abdominal signs and
symptoms or die during follow-up. Therefore, elective revascularization fever. It should be suspected in patients with previous abdominal
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should be considered if they are fit for surgery. surgery, thrombophilia, prior mesenteric or deep venous thrombosis,
cirrhosis, or malignancy.
CLINICAL PRESENTATION OF MESENTERIC ISCHEMIA ■ MISCELLANEOUS CAUSES OF ACUTE MESENTERIC ISCHEMIA
The classic diagnostic triad for chronic intestinal ischemia includes Other pathologic processes occasionally causing acute mesenteric isch-
weight loss, abdominal angina, and altered bowel habit. These patients emia include aortic surgery (when the IMA is ligated and collateral flow
4
are frequently investigated for malignancy before chronic mesenteric is insufficient ), aortic dissection (even when mesenteric vessels are
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