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252 D. Samsami and E. D. Ehrenpreis
Surgical revascularization has been shown to be successful in 84% to 94% of
patients with recurrence rates of 7–14%. Major complications include acute renal
failure (11%), bowel infarction requiring resection (8%), cardiac arrest (6%), respiratory complications (5%), myocardial infarction (5%), and gastrointestinal
hemorrhage (3%).
Endovascular repair includes angioplast y and/or stent placement within the
mesenteric vasculature. Technical success rates are high and reported to be from 90
to 100%. Relapse rates from restenosis are reported to be as high as 28%. These
require repeat endovascular intervention. Major complication rates of endovascular
repair are acute renal failure (6%), infarction requiring bowel resection (3%), and
acute myocardial infarction (3%). Review of the literature shows a better patency
rate with mesenteric artery stenting when compared to angioplasty alone. Stenting
eliminates the possibility of elastic recoil following conventional angioplasty.
Prognosis
Acute ischemic enteropathy has an overall mortality approaching 50%. The prognosis is largely dependent on the mechanism of ischemia as well as treatmen t,
which explains the heterogeneity in numbers reported in the literature. Surgical
repair is considered to have high rate of technical success and can produce
symptomatic improvement in patients with chronic mesenteric ischemia. However,
these surgeries are associated with the significant morbidity and mortality rates of
38% and 13%, respectively. Weight loss and malnutrition, including low albumin
levels, are predictors of increased morbidity and mortality after major surgeries, and
these are common problems in patients with chronic mesenteri c ischemia that
undergo surgical management. Endovascular repair has lower morbidity and mortality rates of 20% and 3%, respectively.
Late deaths, defined as greater than 30 days following mesenteric revascularization, are generally not related to ongoing mesenteric ischemia. A retrospective
review conducted by Tallarita et al. in 2013 evaluated long-term patient survival
and causes of death after open or endovascular revascularization for atherosclerotic
chronic mesenteric ischemia. A total of 343 patients were reviewed and there were
144 late deaths. Reported causes of late death included cardiac conditions (35%),
cancer (15%), pulmonary complications (13%), and mesenteric ischemia (11%).
Recurrent stenosis is a concern following mesenteric revascularization and
occurs in 5–15% of patients. For this reason, routine follow-up is important to
monitor for recurrence of symptomatic disease. It is recommended to have an initial
follow-up imaging study to establish a baseline for future comparison. The imaging
study of choice is a duplex ultrasound. It is repeated at three to six-month intervals
thereafter.
26 Ischemic Enteropathy (Also Called Mesenteric Ischemia) 253
Suggested Reading
1. Fidelman N, Aburahma AF, Cash BD, Kapoor BS, Knuttinen M, Minocha, et al. ACR
appropriateness criteria ® radiologic management of mesenteric ischemia. J Am Coll Radiol.
2017;14(5). https://doi.org/10.1016/j.jacr.2017.02.014.
2. Lo RC, Schermerhorn ML. Mesenteric arterial disease: epidemiology, pathophysiology, and
clinical evaluation. In: Rutherford’s vascular surgery and endovascular therapy, 9th ed. n.d.
Elsevier. p. 1725–34.
3. Danczyk RC, Moneta GL. Clinical evaluation and treatment of mesenteric vascular disease.
In: Vascular medicine: a companion to Braunwalds heart disease, 2nd ed. Philadelphia, PA:
Elsevier/Saunders. p. 328–39.
4. Galandiuk S, Jorden JR, Rice J, Deveaux PG. Acute and chronic mesenteric ischemia. In:
Current therapy in colon and rectal surgery, 3rd ed. n.d. Elsevier. p. 412–7.
5. Brandt LJ, Feuerstadt P. Acute intestinal ischemia. In: Sleisinger and Fordtran’s gastrointestinal and liver disease.
6. Hohenwalter EJ. Chronic mesenteric ischemia: diagnosis and treatment. Semin Intervent
Radiol. 2009;26(4):345–51.
7. Sreenarasimhaiah J. Chronic mesenteric ischemia. Best Pract Res Clin Gastroenterol. 2005;19
(2):283–95.
8. Brandt LJ, Boley SJ. AGA technical review on intestinal ischemia. Gastroenterology.
2000;118:954–68.
9. Management of the diseases of mesenteric arteries and veins clinical practice guidelines of the
European society of vascular disease.
10. Patel R, Costanza M. Mesenteric ischemia, chronic. [Updated 2018 Oct 27]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan.
11. Bala M, Kashuk J, Moore EE, et al. Acute mesenteric ischemia: guidelines of the world
society of emergency surgery. World J Emerg Surg. 2017;12:38. Published 2017 Aug 7.
https://doi.org/10.1186/s13017-017-0150-5.
12. Dang CV, Su M. Acute mesenteric ischemia. https://emedicine.medscape.com/article/189146-
overview. Accessed 3 January 19.
13. Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute mesenteric
ischemia. A clinical review Arch Intern Med. 2004;164(10):1054–62.
14. Mitchell KA, Brian West A. Vascular disorders of the gastrointestinal tract. In: Odze RD,
Goldblum JR, editors. Surgical pathology of the GI tract, liver, biliary tract and pancreas.
Chapter 10, p. 215–255.e3.
15. Harris JW, Mark Evers B. Small intestine. In: Sabiston textbook of surgery. Chapter 49,
p. 1237–95.
16. Tallarita T, Oderich GS, Gloviczki P, Duncan AA, Kalra M, Cha S, Misra S, Bower TC.
Patient survival after open and endovascular mesenteric revascularization for chronic
mesenteric ischemia. J Vasc Surg. 2013;57(3):747–55.
Colonic Ischemia (Also Known as Ischemic Colitis)
Chloe Lee and Eli D. Ehrenpreis
Introduction
Colonic ischemia is a condition that results when blood flow to the colon is
compromised, causing an inability to mai ntain adequate colonic tissue perfusion
and nutrition. This physiologic dysfunction can lead to ischemic damage and
reperfusion injury, resulting in eith er reversible or irreversible damage. Although
most cases are self-limited, treatment for each patient should be tailored to severity
of presentation and associated risk factors.
Epidemiology
27
CI is the most frequent form of intestinal ischemia. The incidence of CI based on a
national insurance claims-based survey was estimated to be 17.7 cases per 100,000
person-years. CI occurs in adults of all ages but it is more common in women and in
the older population of patients in their sixties and seventies. However, younger
individuals may develop CI in settings of hypercoagulable states, drug-induced
conditions and collagen vascular diseases.
C. Lee
Department of Internal Medicine, Advocate Lutheran General Hospital,
1775 Dempster St, 6 South, Park Ridge, IL 60068, USA
E. D. Ehrenpreis (&)
Department of Medicine, Advocate Lutheran General Hospital,
1775 Dempster St, 6 South, Park Ridge, IL 60068, USA
e-mail: e2bioconsultants@gmail.com
© Springer Nature Switzerland AG 2021
E. D. Ehrenpreis et al. (eds.), The Mesenteric Organ in Health and Disease,
https://doi.org/10.1007/978-3-030-71963-0_27
255
256 C. Lee and E. D. Ehrenpreis
Risk Factors
A variety of conditions are associated the development of CI (Table 27.1). Patients
of advanced age who have accompanying comorbid conditions are at especially
high risk of developing CI. Hypertension, diabetes mellitus, coronary artery disease, dyslipidemia, chronic obstructive pulmonary disease, congestive heart failure,
atrial fibrillation, and renal disease are comorbidities that are associated with the
development of CI. Notably, coronary artery disease and atrial fibrillation were
approximately twice as common in patients with right colon ischemia compared
with ischemia in other segments of colon. A variety of surgeries can result in
compromised arterial blood flow to the colon, including abdominal aortic aneurysm
repair, cardiopulmonary bypass and renal transplantation. Colonos copy and barium
enema as well as a variety of medications and illicit drugs are other iatrogenic
factors that are associated with the development of CI. Patients with irritable bowel
syndrome (IBS) have been determined to have an increased risk for CI, possibly as
a consequence of excessive sympathetic activity in the mesenteric vasculature.
Severe constipation is a risk factor for CI and is also associated with a segmental
form of colonic ischemia termed stercoral ulcers. These are due to pressure on the
colonic wall and decreasing blood flow that is obstructed by hard stool. Thrombophilia is another risk factor for CI. Younger patients with CI should be evaluated
for hereditary coagulopathies such as Factor V Leiden mutation and deficiencies of
protein C, protein S and antithrombin III. Of interest, hematochezia and endoscopically diagnosed right sided IC has been described in long distance runners,
particularly in females. Pharmacologic agents including vasoconstrictors, psychotropics, oral contraceptives, Type 1 interferon, 5-hydroxytrptamine-1 (5-HT1)
agonists, and illicit drugs are known causes of nonocclusive CI (Table 27.2).
Despite a long list of possible causes of CI, many patients with CI will have no
identifiable risk factors for the disease.
Pathophysiology
CI is caused by a sudden reduction in blood flo w to the mesenteric vasculature and
subsequent decrease in oxygen to regions of the colon. The large intestine receives
its blood supply from the superior mesenteric artery and inferior mesenteric artery,
while the rectum has a dual blood supply that includes the inferior mesenteric artery
and the internal iliac arteries. The “watershed” regions of the colon include the
splenic flexure (Griffith’s point), the joining point where the blood supplies of the
superior mesenteric artery and inferior mesenteric artery meet and part of sigmoid
colon (Sudeck’s point), where the blood supplies of the inferior mesenteric arteries
and rectal arteries connect. These areas are at increased risk for ischemia due to
limited collateral blood flow (Fig. 27.1). Nonocclusive ischemia is the most common mechanisms for the development of CI. The degree of systemic perfusion and
collateral circulation determine the overall development of hypoxia and subsequent
27 Colonic Ischemia (Also Known as Ischemic Colitis) 257
Table 27.1 Medical risk factors for colonic ischemia
Occlusive disease Nonocclusive disease
Arterial Hypoperfusion state
Thrombosis Congestive heart failure
Cardiac emboli Pancreatitis
Cholesterol emboli Hypotension
Small vessel disease Shock
Diabetes Hemodialysis
Vasculitis Pharmacologic
Atherosclerosis Medications
Amyloidosis Illicit drugs
Rheumatoid arthritis Gastrointestinal
Radiation Irritable bowel syndrome (IBS)
Venous Constipation
Mesenteric venous thrombosis
Portal hypertension
Hypercoagulable state
Lymphocytic phlebitis
Surgical
Aortoiliac reconstruction
Cardiopulmonary bypass
Colectomy
Colonoscopy
Barium enema
Renal transplant
Modified from Washington, Christopher, and Joseph C. Carmichael. “Management of Ischemic
Colitis.” Clinics in Colon and Rectal Surgery 25.4 (2012): 228–235. Reused with permission
Copyright © Thieme
reperfusion. The most common etiologies of nonocclusive CI include sepsis,
hemorrhage and heart failure. During shock states, there is redistribution of blood
flow to the systemic circulation and away from the splanchnic circulation.
Hypoperfusion of the colon enhances the risk of ischemic injury due to increased
demand in setting of preexisting diminished circulation. It is thought that
renin-angiotensin axis is involved in the splanchnic v asoconstriction that occurs in
response to shock. Various medications are also known to cause vasospasms
leading to nonocclusive CI.
Traditionally, CI is also divided into gangrenous and non-gangrenous forms with
the latter accounting for 80–85% of cases. Gangrenous CI requires surgical intervention. Further classification defines CI into Type I or II disease. Type I disease
refers to idiopathic, nonocclusive ischemia likely due to small vessel disease. These
patients are generally managed with supportive care. Type II disease is associated
258 C. Lee and E. D. Ehrenpreis
Table 27.2 Pharmacologic risk factors for ischemic colitis
Drugs
Moderate evidence
Constipation inducing drugs
Immunomodulator drugs (Antitumor necrosis factor-alpha, Type 1 interferon)
Illicit drugs (amphetamines, cocaine)
Low evidence
Antibiotics
Appetite suppressants
Chemotherapeutic drugs
Decongestants
Diuretics
Ergot alkaloids
Hormonal therapies
Laxatives
Psychotropic drugs
Serotoniergic drugs
Very low evidence
Digitalis
Kayexalate
Non-steroidal anti-inflammatory drugs (NSAIDs)
Statins
Adapted from: Brandt, Lawrence. ACG Clinical Guideline: Epidemiology, Risk Factors, Patterns
of Presentation, Diagnosis, and Management of Colon Ischemia. AM J Gastroenterol 2015;
110:18–44. Copyright © Wolters Kluwer 2015
with an identified etiology and usually followed by systemic hypotension,
decreased cardiac output or aortic surgery.
The left colon is the segm ent most affected with CI, and accounts for 32.6% of
patients with the disease. CI occurs in the distal colon 24.6%, right colon 25.2% and
entire colon 7.3% of the time. It has been shown that patients with right sided CI
have a poorer outcome than those with CI occurring in any other segments of the
colon. Figure 27.1 shows the watershed regions of the colon.
CI is usually a transient, self-limited condition. However, stricturing and prolonged colonic inflammation can occur as long-term complications of the disease.
Clinical Presentations
Clinical manifestations of CI are highly variable. In general, patients with CI
develop sudden lower abdominal cramping and the urge to defecate. This is often
accompanied by the passage of bloody diarrhea, usually within 24 hours of the
27 Colonic Ischemia (Also Known as Ischemic Colitis) 259
Aorta
Left phrenic a.
Right phrenic a.
Celiac trunk
Pancreatico-
duodenal a.
SMA
IMA
IIA
Hemorrhoidal aa.
Superior
Middle
Inferior
Splenic a.
Griths’ point
Arch of riolan
Marginal a.
Sudeck’s
point
Fig. 27.1 Watershed regions of the colon
onset of abdominal pain. Although blood loss in CI is usually mild, severe anemia
due to excessive hemorrhage can occur and are often associated with gangrenous CI
and/or fulminant pancolitis. Other nonspecific symptoms occurring in patients with
CI include fever, nausea, vomiting, anorexia and presyncope.
Relatively mild tenderness of the abdomen, sometimes at the region of the
affected segment of the colon is found on physical examination. Severe tenderness
with peritoneal signs suggests the presen ce of advanced disease, including
260 C. Lee and E. D. Ehrenpreis
peritonitis. In addition, severe cases of CI can demonstrate signs of overwhelming
infection including high fever, tachycardia and hypotension.
In most patients, signs and symptoms of the disease are transient and
self-limited. More than half of the patients with CI have resolution of their
symptoms within 2–3 days. Later recurrences of CI are relatively uncommon and
are seen in 6.8–16% of patients. The rates of complicated CI are 14.3% for stricture
formation, 9.9% for gangrenous colitis and 2.5% for fulminant colitis.
Diagnosis
Because of the nonspecific nature of symptoms of CI, the large differential diagnosis for the common presentations of CI and the fact that CI is often idiopathic, a
high index of suspicion for mesenteric ischemia, including CI, should be entertained in patients with abdominal pain and rectal bleeding. Nonetheless, establishing the diagnosis and severity of CI often requires an assessment of findings
from the medical history (including risk factors), physical examination, laboratory
testing, imaging and endoscopic evaluation of the colon. Computerized tomography
(CT) of the abdomen is frequently performed in patients with abdominal pain
and/or gastrointestinal bleeding. Colonoscopy is generally performed within
48 hours and can confirm colonic ischemia based on its typical appearance and
biopsy confirmation.
Laboratory Findings
Although laboratory studies are neither sensitive nor specific for CI, they can help
predict the severity of CI. Elevated white blood cell count, lactate dehydrogenase
(LDH) and decreased hemoglobin (Hgb) concentration occur commonly in patients
with CI. Serum levels of D-lactate may be a marker for CI. Severe cases of CI have
characteristic laboratory findings. These include elevated serum lactate levels, the
presence of metabolic acidosis, and a significant base deficit usually accompanied
by profound anemia. Since hematochezia with or without abdominal pain may be
infectious in origin, stool studies for culture, ova and parasite exam, and
Clostridium toxin assay are included in patient evaluation.
Imaging
Plain films of the abdomen can show “thumbprinting,” representing edema or
thickening of the bowel in early ischemia (Fig. 27.2). CT of the abdomen with
intravenous contrast is usually the imaging of choice with high suspicion for CI.
Findings may include colon wall thickening and luminal narrowing, although these
findings are nonspecific (Fig. 27.3).
27 Colonic Ischemia (Also Known as Ischemic Colitis) 261
Fig. 27.2 AP abdominal
radiograph of a different
patient shows the plain film
appearance of
“thumbprinting” involving the
descending colon (asterisks)
Fig. 27.3 Coronal and axial
contrast-enhanced computed
tomography images with wall
thickening and irregular
luminal narrowing of the
transverse colon (oval),
indicative of a nonspecific
focal colitis. Colonoscopy and
pathology confi rmed the
diagnosis of ischemic colitis.
With permission from Dr.
Abraham Dachman and Dr.
Justin Ramirez
262 C. Lee and E. D. Ehrenpreis
Fig. 27.4 Axial computed tomography image demonstrates branching radiolucencies (circle)
within the hepatic parenchyma compatible with portal venous gas. Additional foci are present at
the periphery of the right hepatic lobe and adjacent to the middle hepatic vein and IVC. Incidental
note of contrast filled hiatal hernia (asterisk)
Contrast enhanced CT and CTA have high sensitivity and specificity for
assessing vascular occlusion as an etiology of CI, although it is generally not
required since most cases are due to non-occlusive disease. Presence of pneumoperitoneum and hepatic portal venous gas indicate bowel necrosis although
surgical manipulation can also cause such finding (Figs. 27.4 and 27.5). Pneumatosis intestinalis is a radiological finding of gas bubbles within the mucosa or
submucosa of the intestinal wall most commonly associated with bowel ischemia.
Mucosal disruption from bowel ischemia, systemic infection, or inflammation may
lead to the development of pneumatosis intestinalis. US and MRI are less used
imaging modalities in diagnosis of CI.
Colonoscopy
Colonoscopy with biopsy is the most accurate means of diagnosing CI. It provides
the means to directly visualize the abnormal colonic mucosa and allow tissue
collection for histology. Necrotic mucosa can be identified by the presence of a
dusky and/or cyanotic discoloration in affected segments of colon. If necrosis is
identified, immediate removal of the colonoscope, and consideration of rapid surgery is required. Early colonoscopy (within 48 hours of presentation) is recommended in most patients who are suspected to have CI.
The location of abnormal mucosa can also be determined. Severe and gangrenous forms of the disease may be identi fied and require immediate withdrawal of
the colonoscope. The presence of submucosal hemorrhage in the splenic flexure is a