Small Bowel

Educational Objectives

The goal of this program is to improve diagnosis and medical and surgical treatment of small bowel ischemia and Clostrid­ium difficile colitis. After hearing and assimilating this program, the clinician will be better able to:

1.   Diagnose acute mesenteric insufficiency.

2.   Identify characteristics and common symptoms of patients with chronic and acute mesenteric ischemia.

3.   Explain the relationship between duration of acute mesenteric insufficiency and viability of the small bowel.

4.   Discuss the options for surgical management of acute and chronic mesenteric ischemia.

5.   Describe diagnostic testing for identification of
C difficile colitis.

Faculty Disclosure

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the plan­ning committee to disclose relevant financial relationships within the past 12 months that might create any personal con­flicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, the faculty and planning committee reported nothing to disclose.

Acknowledgments

Dr. Grove was recorded at Surgery of the Foregut, held February 15-18, 2009, in Miami, FL, and presented by the Cleveland Clinic Florida in conjunction with the German Society of Visceral Surgery, the Federation of Latin American Surgeons, the European Surgical Institute, and the Latin-American Society of Endoscopic Surgeons. Drs. Santilli and Trudel spoke at Ad­vances in Gastrointestinal and GI Laparoscopic Surgery, held June 10-13, 2009, in Minneapolis, MN, and sponsored by the University of Minnesota Medical School. The Audio-Digest Foundation thanks the speakers and the sponsors for their co­operation in the production of this program.

Approach to Small Bowel Ischemia

Mark K. Grove, MD, Staff Physician, Department of Vascular Surgery, Cleveland Clinic, Weston, FL

Diagnosis of acute arterial insufficiency: etiology  —  arterial embolism and thromboses in »50% of patients; nonocclu­sive ischemia, venous thrombosis (VT), and miscellaneous causes in remaining 50%; when evaluating patient, no practical difference between embolic or thrombotic occlusion

Patient history and presentation: ask about risk factors for or history of atherosclerosis; embolus often spares first jeju­nal branches off superior mesenteric artery (SMA), so ischemia may not affect entire small bowel; not true in pa­tients with thrombosis (entire small bowel becomes ischemic); patients often older; chronic congestive heart failure or atrial fibrillation significant risk factors; may be detected in association with acute illness (eg, myocardial infarc­tion, burn, trauma) most patients report abdominal pain disproportionate to physical findings; patients sometimes describe forceful bowel evacuation at onset

Physical examination: early findings often nonspecific; initial abdominal findings may be minimal; patients with progression to hemodynamic instability, abdominal distension, or peritoneal signs may be unsalvageable; per­form rectal examination for occult bleeding

Clinical evaluation: severe acidosis may be indicator, but few other laboratory results useful for diagnosis; white blood cell (WBC) count often elevated; patient may be azotemic due to dehydration or blood in gastrointestinal (GI) tract; imaging studies  —  obtain quickly (greater utility in diagnosis); plain abdominal film may show evi­dence of pneumoperitoneum or pneumatosis; computed tomography (CT) angiography and contrast angiography are mainstays of radiologic diagnosis; duplex ultrasonography and magnetic resonance angiography (MRA) not helpful in acute setting; CT found to have 100% sensitivity, 89% specificity for acute mesenteric insufficiency (test of choice for evaluating superior mesenteric venous [SMV] thrombosis); arteriography gold standard for di­agnosing acute mesenteric insufficiency (perform early); obtain lateral as well as anteroposterior films

Timing of intervention: upon diagnosis, “clock is ticking”; study  —  intestinal viability inversely correlated with du­ration of ischemic symptoms; nearly all patients treated within 12 hr had viable intestine; of patients treated within 12 to 24 hr, slightly >50% had viable intestine; >80% of patients with diagnosis made >24 hr after symp­tom onset had mesenteric infarction; risk for mortality triples in patients with nonviable bowel; patients often go directly from angiography lab to operating suite; all diagnosed patients should receive intensive monitoring, on­going fluid resuscitation, antibiotics, and anticoagulation

Endovascular intervention: options for thrombolytic therapy include mechanical or chemical thrombolysis; draw­backs include time required for chemical thrombolysis and inability to evaluate bowel viability; recommended by American College of Cardiology only for selected patients (surgery still considered best option for patients with acute arterial insufficiency)

Surgical options: finding SMA may be difficult in pulseless vessel (expose through cephalad retraction of transverse me­socolon); simple embolectomy indicated for patients with embolus (transverse or longitudinal arteriotomy); consider retrograde operative mesenteric stenting at origin of proximal SMA; retrograde bypass using autologous conduit (eg, saphenous vein) considered standard treatment; if questions remain about viability of intestine after revascularization, perform second laparotomy within 12 to 24 hr

Postoperative care: reperfusion may cause massive swelling of bowel and resultant ascites; watch for ongoing isch­emia; provide nutritional support; find source of embolism; mortality associated with acute ischemic mesenteric event averages 71% (not significantly improved over last 75 yr)

Chronic mesenteric ischemia: patients often older women; commonly smokers, with other signs of atherosclerotic dis­ease; classic signs include fear of eating and associated weight loss; patient may have undergone cholecystectomy or multiple diagnostic studies, including noninvasive imaging studies; surgical options include retrograde bypass (vascular surgeons usually prefer antegrade bypass); bifurcated graft indicated in some cases; reported mortality rates 6% to 11%; reconstruction associated with 90% patency; 5-yr survival 70%; endovascular management asso­ciated with 10% mortality rate (comparable to surgery)

Mesenteric Vascular Disease of the Small Bowel

Steven M. Santilli, MD, PhD, Professor and Chief, Division of Vascular and Endovascular Surgery, University of Minnesota Medical School, Minneapolis

Chronic Mesenteric Ischemia

Introduction: symptomatic visceral ischemia rare; considered poor prognostic sign for survival; etiology  —atherosclerosis or celiac access compression syndrome

Atherosclerosis: collateral visceral circulation usually compensates for ischemic vessel; 30% of patients with athero­sclerosis have significant stenosis of ³1 visceral artery; without history of previous abdominal surgery (ie, no dis­ruption of collateral pathways), clinical syndrome requires occlusion of 2 or 3 visceral arteries

Patient characteristics: women outnumber men 3 to 1; average age 59 yr; average duration of symptoms 18 mo

Symptoms and signs: typically, dull deep cramping abdominal pain that begins 15 to 30 min postprandially and lasts 1 to 3 hr; pain intensity directly related to size of meal; eventually results in food aversion and significant weight loss; bowel movements usually normal; on examination, patients usually have diffuse atherosclerosis, ap­pear thin and cachectic, and have abdominal bruit

Diagnosis: duplex ultrasonography effective if laboratory experienced, but not recommended as sole method of diag­nosis; MRA and CT effective for visualization of visceral artery anatomy; angiography considered gold standard; arteriography may permit both diagnosis and treatment

Treatment: endovascular  —  stenting usually associated with good results; surgical  —  antegrade bypass to 1 or 2 ves­sels; retrograde bypass (gaining in popularity; patency rate similar to those achieved with antegrade bypass); throm­boendarterectomy effective in experienced hands, but physiologically stressful for patient; in speaker’s comparison of surgical and endovascular therapy, surgery associated with higher mortality rate; morbidity not reported (in other series, surgery associated with “substantially higher” morbidity); long-term patency rates similar; results of endo­vascular treatment improved when stenting used; conclusion  —  “endovascular therapy for chronic mesenteric isch­emia is first-line treatment”

Celiac access compression syndrome: controversial; diagnosis of exclusion; at University of California, San Fran­cisco, best treatment outcomes (60%-70% improvement) achieved with female patients 40 to 60 yr of age with postprandial pain, weight loss >20 lb, no history of psychiatric disorder or drug abuse, and anatomic findings of high-grade proximal stenosis with poststenotic dilatation

Anatomy: median arcuate ligament of diaphragm compresses proximal celiac access

Diagnosis: gold standard is arteriography; CT or MR angiography possibly adequate

Treatment options: divide median arcuate ligament (many patients have intrinsic arterial pathology requiring patch), or perform antegrade bypass

Acute Mesenteric Ischemia

Presentation: patients mostly women; report acute abdominal pain and descended abdomen; 50% of patients experi­ence vomiting; one-third have diarrhea; classic finding is pain out of proportion to physical examination; 25% of patients have occult GI bleeding; mortality high in most series

Causes: most common include arterial occlusion from emboli or acute on chronic conditions, nonocclusive mesen­teric ischemia, and VT

General treatment guidelines: patients with peritonitis require immediate surgery; if history and physical examination suggestive of occlusion and bowel salvageable, immediate intervention recommended; perform arteriography if his­tory and physical suggest nonocclusive mesenteric ischemia

Embolization: sources usually cardiac (incidence falling, but still most common) or arterioarterial; patients have no history of symptoms consistent with chronic visceral ischemia and few (if any) manifestations of systemic athero­sclerosis; SMA usually involved; embolus usually lodges at branch point where SMA narrows; arteriography usu­ally shows normal SMA with acute cutoff and intraluminal filling defect; treat with embolectomy (usually successful)

Acute on chronic mesenteric ischemia: patients usually have long history of chronic mesenteric ischemia, then sud­denly develop severe unrelenting abdominal pain (suggests high-grade visceral artery stenosis that progressed to thrombosis and occlusion); other sequelae of atherosclerosis usually present; arteriography shows diseased aorta and iliac arteries with no filling of SMA; if diagnosed during arteriography, attempt endovascular therapy (balloon angioplasty or stenting; thrombolysis too slow); if no response to endovascular therapy, proceed to surgery for re­vascularization; surgical treatment  —  retrograde bypass from infrarenal aorta or iliac arteries; revascularization of 2 vessels recommended; if bowel resection necessary, conduit of choice is autologous tissue from saphenous vein

Nonocclusive mesenteric ischemia: normally occurs in patients with severe multisystem illness and low-flow states (eg, severe congestive heart failure); patients usually on vasopressors; also associated with cocaine abuse; difficult to diagnose in sedated intubated patients (maintain high index of suspicion; proceed to arteriography); treatment  —vasodilator infusion into visceral artery; proceed to surgery if patient develops peritonitis

Venous thrombosis: usually seen in older patients; incidence equal in men and women; patients usually present with generalized abdominal pain and occult GI bleeding; accounts for 5% to 15% of cases of acute mesenteric isch­emia, but should be considered in patients with history of, eg, deep venous or portomesenteric thrombosis; most patients have secondary source of VT (eg, hypercoagulable state, history of previous splenectomy or sclerother­apy); acute mortality rates high; long-term survival rates low due to underlying medical condition

Diagnosis: look for indirect indicators; CT angiography  —procedure of choice; may show large thrombosed vein, vein with filling defects, or pneumatosis intestinalis; triad of SMV thrombus, thickened small intestinal wall, and peritoneal fluid “highly suggestive of bowel infarction” and need for laparotomy; MR imaging with gadolinium possibly equivalent option

Treatment: vigorous resuscitation, broad spectrum antibiotics, long-term anticoagulation, and identification of under­lying cause; results of thrombolytic therapy mixed and associated with significant risk for bleeding; explore and re­sect bowel as indicated; assessing bowel viability  —fluorescein with Wood’s lamp (most accurate); clinical judgment; Doppler imaging (least accurate)

Medical and Surgical Treatment
for Clostridium Difficile Colitis

Judith L. Trudel, MD, Clinical Professor of Surgery, University of Minnesota Medical School, Minneapolis

Presentation and pathophysiology: illness results from toxin secreted by organism; asymptomatic carriers may transmit C difficile through spores or oral-fecal route; C difficile-associated disease (CDAD) most common cause of nosocomial diarrhea in United States; exposure to antibiotics greatest risk factor; advanced age and hos­pitalization also increase risk; current form of CDAD more prevalent and aggressive than that seen before 2000; due largely to new strain in North America; produces greater quantities of toxins A and B than older strain and additional binary toxin that increases effects of other 2; also produces collagenase, which results in mucosal breakdown and bacterial translocation; incidence increasing in patients without exposure to antibiotics (those on immunosuppressants or chemotherapy; elderly patients)

Physical examination: nonspecific, unless disease advanced

Diagnosis: based primarily on finding toxin in stool (toxin B usually sought); pseudomembranes  —  raised whitish or yel­lowish plaques adhering to underlying mucosa; found in <50% of patients with toxin-positive CDAD; absence does not rule out disease; distribution patchy (flexible sigmoidoscopy recommended, but plaques may occur only above trans­verse colon [ie, in inaccessible regions]); stool cultures  —  not generally performed (results take several days; asymp­tomatic carriers confound diagnosis; sensitivity of assay for toxin 70% to 90% [but highly specific]); CT  —  findings usually nonspecific; ileus and thickened bowel possible

Medical treatment: stop antibiotics (when appropriate); use of antiperistaltic agents discouraged (slowing peristalsis allows toxin to accumulate in colon; increases risk for toxic megacolon or perforation); oral metronidazole inex­pensive and usually effective, although efficacy now diminishing; if ineffective, repeat course of metronidazole, or switch to vancomycin; results with probiotics mixed; toxin-binding agents not recommended as first-line ther­apy; cholestyramine (eg, Questran, Cholybar) binds toxin, but also binds vancomycin

Recurrent disease: due to residual spores or new infection; no known antibiotic-resistant strains of C difficile, so re­peated courses may be indicated; fecal bacteriotherapy, immunoglobulins, and toxoid vaccines last choices

Surgery: indicated for most severe cases; procedure is subtotal or total abdominal colectomy (TAC) with end ileos­tomy; TAC associated with lowest mortality rate; candidates  —  older, hospitalized, immunosuppressed (often septic) patients, and those in organ failure; patients with inflammatory bowel disease (IBD) highly susceptible to CDAD (treating IBD with steroids and immunosuppressants may exacerbate CDAD)

Impact on survival: strongest predictors of mortality include WBC count >50,000, lactate >5 mmol/L, shock requiring vasopressors, advanced age, and immunosuppression; mortality associated with medical treatment alone signifi­cantly higher than that with emergency colectomy; survival highest when surgery performed before patients reach above parameters

Suggested Reading

Assar AN, Zarins CK: Acute mesenteric ischaemia: facts and perspectives. Br J Hosp Med (Lond) 69:686, 2008; Cangemi JR, Picco MF: Intestinal ischemia in the elderly. Gastroenterol Clin North Am 38:527, 2009; Dudukgian H et al: C. difficile colitis  —  predictors of fatal outcome. J Gastrointest Surg 14:315, 2010; Eltarawy IG et al: Acute mesenteric ischemia: the im­portance of early consultation. Am Surg 75:212, 2009; Kougias P et al: Determinants of mortality and treatment outcome fol­lowing surgical interventions for acute mesenteric ischemia. J Vasc Surg 46:467, 2007; Mell MW et al: Outcomes after endarterectomy for chronic mesenteric ischemia. J Vasc Surg 48:1132, 2008; Noblett SE et al: The role of surgery in Clostrid­ium difficile colitis. BMJ 338:b1563. Doi: 10.1136/bmj.1563. May 2, 2009; Resch TA et al: Endovascular techniques in acute arterial mesenteric ischemia. Semin Vasc Surg 23:29, 2010; Schermerhorn ML et al: Mesenteric revascularization: manage­ment and outcomes in the United States, 1988-2006. J Vasc Surg 50:341, 2009; Vokurka J et al: Acute mesenteric ischemia. Hepatogastroenterology 55:1349, 2008; Zeller T et al: Endovascular therapy of chronic mesenteric ischaemia. EuroInterven­tion 2:444, 2007.