VASCULAR SURGERY
| CHRONIC MESENTERIC ISCHEMIA —Nikhil Kansal, MD, Assistant Professor of Surgery and Director, Endovascular
Surgery, Section of Vascular and Endovascular Surgery, University of California, San Diego, Medical Center
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| Chronic mesenteric ischemia (CMI): defined as chronic lack of blood flow to visceral (celiac, superior mesenteric,
and inferior mesenteric) arteries; classic symptom complex triad of postprandial abdominal pain, weight loss, and fear of
eating; diagnosis difficult; can be caused by variety of visceral conditions, including atherosclerotic stenosis or occlusion
of arteries (most common); embolism; celiac artery compression syn-drome; nonocclusive mesenteric ischemia (MI);
mesenteric venous thrombosis
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| Associated conditions: neurofibromatosis; fibromuscular disease; Buerger’s disease; polyarteritis nodosa; ergot poisoning;
cocaine abuse
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| Conditions with similar signs and symptoms: peptic ulcer disease; gallbladder disease; appendicitis; inflammatory
bowel disease; gynecologic pathology; hiatal hernia; gastroesophageal reflux
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| Pathophysiology: occlusion or stenosis of visceral arteries—occlusive process (atherosclerotic plaque) commonly
occurs at ostia of visceral arteries; efficient collateral circulation between arteries; while stenosis of visceral arteries not
rare, symptomatic stenosis is (in general, at least 2 of 3 major visceral arteries must be significantly stenotic or occluded
before symptoms occur; symptoms can occur with solitary superior mesenteric artery [SMA] lesion if collateral circulation
interrupted); postprandial intestinal hyperemia—normally, dynamic increase in visceral blood flow to intestine
after food bolus (meal); lack of increase in blood flow leads to symptoms of intestinal ischemia
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| Signs and symptoms: most patients 40 to 70 yr of age; women-to-men ratio 3:1; symptoms—midabdominal or epigastric
pain (colicky or dull in nature; occasionally radiates to back; usually associated with food bolus; begins 15-30 min after
meal; lasts 1-3 hr; no associated peritonitis; varies with size of meal); signs—significant weight loss (hallmark of
CMI); abdominal bruit; few other signs that can be seen on physical examination
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| Diagnosis: often diagnosis of exclusion; most patients present after numerous diagnostic tests; high index of suspicion important;
imaging tests—duplex ultrasonography (primarily screening tool; operator dependent); magnetic resonance angiography
(MRA; newer modality; tends to overestimate stenosis); computed tomography (CT; better image quality,
especially with fine cuts; multislice detectors able to show more detail; may replace contrast arteriography in future); contrast
arteriography (currently gold standard for identifying anatomic stenosis or occlusion; invasive; contrast-induced risk
for nephropathy; therapeutic intervention can be performed at time of diagnosis)
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| Surgical bypass: gold standard for treatment; antegrade or retrograde; inflow—for antegrade bypass, inflow artery either
supraceliac or descending thoracic aorta (if supraceliac calcified or unfavorable donor); for retrograde bypass, inflow artery
either infrarenal aorta or iliac artery (whichever easier); alternative inflow arteries; conduit—in general, autogenous (vein)
conduit preferred (especially in younger patients), depending on length of bypass (eg, prosthetic conduit probably less prone
to kinking, and patency may be similar to that of vein); outflow—involves revascularization of celiac artery, SMA alone, or
both; retrograde bypass potentially advantageous (eg, possibly lower morbidity and mortality, easier to perform) but also
potentially problematic (eg, must know how to perform, excludes celiac reconstruction); antegrade bypass ideal if planning
to do dual reconstruction (allows access to celiac artery and SMA; can be done retroperitoneally or transperitoneally)
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| Endarterectomy: transaortic—utilizes “trap door” aortotomy; primarily treats orificial lesions; also can be used to
treat renal artery stenosis; requires significant experience; direct—usually done if only one artery involved; useful for
midarterial (but not orificial) lesions
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| SMA-celiac artery reimplantation: technically difficult; rarely used
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| Angioplasty and stenting: emerging modality for treating visceral artery stenosis; initial short-term morbidity and mortality
lower than with major laparotomy; access usually via brachial artery; inferior patency, compared to surgical bypass (patients
must be monitored; surveillance usually done via duplex ultrasonography); risk for embolization during procedure may
be minimized with use of embolic protection device; reasonable approach for poor candidate for open surgical procedure (not
recommended for young healthy patient with good life expectancy)
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| Celiac artery compression syndrome: etiology—abnormally low median arcuate ligament in presence of normally
positioned celiac axis and SMA; periarterial splanchnic nerve plexus around celiac artery may contribute to pain and to
symptomatology; presentation similar to MI; diagnosis also one of exclusion (established by arteriography with inspiration
and expiration); treatment—midline or subcostal laparotomy (expose surface of celiac artery; transect arcuate ligament;
doing sharp dissection, skeletonize periarterial splanchnic neural tissue); done open or laparoscopically; persistent
stenosis often seen after removal of tissue (corrected with dilator, balloon angioplasty, or surgical bypass)
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| Mesenteric venous thrombosis: seen in 15% of all patients with MI; significant mortality; etiology—sometimes no
identifiable primary cause (or may be unidentified hypercoagulable state); secondary causes include endothelial injury,
stasis in venous system, hypercoagulable states, and direct injury to vein; description of pathophysiology; clinical
presentation—subacute progression (develops in days to weeks; onset insidious); nonspecific symptoms (peritoneal
signs in 16% of patients; pain out of proportion to examination; tenderness unimpressive if patient does not have peritonitis;
many patients have guaiac-positive stools and leukocytosis); diagnosis—CT probably gold standard (good sensitivity
and specificity; early diagnosis with increasing use of CT has improved clinical outcomes); angiography another option
(not as ideal as CT); management—anticoagulation (intraoperative or perioperative) primary treatment; duration depends
on etiology of venous thrombosis; laparotomy required in patients who have peritonitis (resect grossly involved
bowel; second look not routinely necessary); close clinical follow-up required
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| Nonocclusive MI: ischemia in absence of mechanical vascular obstruction; not usually chronic; typically due to circulatory
insufficiency or end-organ shock (can be drug-induced with vasoactive agents); etiology—severe prolonged visceral
vasospasm; normal compensatory vasodilation in response to shock does not occur; accounts for 20% of patients
with MI; seen in patients with severe multisystem illness in setting of low-flow states (eg, patients with congestive heart
failure [CHF] or cardiogenic shock); patients often on high-dose or significant vasoconstrictor therapy; most already
have sepsis, dehydration, renal, and/or hepatic disease; signs and symptoms similar to those of ischemia; diagnosed by
angiography; treatment—primarily nonoperative (must treat underlying disease process, optimize fluids and cardiac
output, and eliminate vasoconstrictor medications as tolerated; vasodilators not helpful; anticoagulation recommended);
angiography can be done in stable patient who is normovolemic; laparotomy reserved for patients who are unstable or
who have peritonitis; patient survival poor
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| MANAGEMENT OF THE INFECTED DIABETIC FOOT —Diane D. Branks, DPM, Vascular Division, Kaiser Permanente
–Southern California Permanente Medical Group, Baldwin Park, CA
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| Background: 20.8 million diabetics in United States; 15% of all diabetics develop foot infections at some point during
lifetime; 20% of diabetic foot hospitalizations related to infection; 16% of patients with foot ulcers eventually have lower
extremity amputation (LEA); in 60% of LEAs done in United States, diabetic foot infection predisposing factor
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| Risk for infectious disease in diabetic patients: 2003 study found patients with diabetes had greater incidence of
hospitalization or physician claim for infectious disease (50% vs 38%), 80% greater risk for cellulitis, 4-fold greater risk
for osteomyelitis, and 2-fold greater risk for sepsis than nondiabetic patients; also, death from infectious disease more
prevalent; diabetic patients have more comorbidities that put them at higher risk for infections and other medical complications;
according to American Diabetic Association and American College of Cardiology, those at high cardiovascular
risk have resultant increase in peripheral vascular risk factors
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| Causes of diabetic foot problems: neuropathy—typical “stocking-glove” neuropathy causes numbness or lack of
feeling; motor neuropathy causes atrophy of intrinsic muscles of foot, leading to development of claw toes (which have
tendency to rub inside shoes and create ulcers); autonomic neuropathy associated with increased risk for anhydrosis in
foot and fissuring (can lead to infections); tricep weakness—causes drop foot and puts forefoot at high risk for ulceration;
when combined with peripheral arterial disease, these patients at extremely high risk for limb loss
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| Comment: toxicity does not express itself in diabetics as well as it does in nondiabetics (often, patients present with massive
foot infections but complain only of flu-like symptoms); be aware that they may not have high white blood cell
count, and will not have complaint of fever (only 50% with massive infection have temperature >100°F)
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| Classification of diabetic foot infections: classification system and treatment guidelines soon to be published; useful
in helping clinicians decide when to hospitalize, when to use parenteral vs oral antibiotics, and when urgent surgery
required; currently, most clinicians describe infections as mild, moderate, limb-threatening, or non–limb-threatening; patient
with limb-threatening infection typically has fever, malaise, leukocytosis, hyperglycemia (may have cellulitis >2
cm, lymphangitis, edema, bacteremia, deep-space infections, bone or joint fascia abscess, gangrene, or necrotizing fasciitis)
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| Management: sharp debridement cornerstone of treatment; follow tendons up foot into leg, looking for any pockets or
areas in which infection may be tracking; speaker does aggressive flushing of infected areas (pulse lavage used in operating
room; on floor, nurses do 3-times-daily aggressive flushing and packing immediately after incision and drainage [I
and D]; large amount of surgical scrub used [keeps bacteria count down]); deep infection in foot always requires admission
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| Timing of I and D: perform I and D “sooner rather than later”; study by Faglia et al compared patients who underwent
immediate I and D to group that did not undergo procedure until after hospital stay of 6 to 13 days; logistical analysis of
data showed that for every delay in debridement, risk for amputation increased 1.6-fold
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| Causative pathogens: severe infections typically polymicrobial, mild infections monomicrobial; Staphylococcus aureus
most common bacteria in foot infections, Enterococcus second most common; Pseudomonas not common pathogen
in diabetic foot; major emerging pathogen methicillin-resistant S aureus (MRSA); recent study found death rate 2.5
times greater in patients with MRSA (vs other foot infections); MRSA infection approximately 3 times more expensive
to treat (median cost $35,000)
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| Diagnosis of underlying osteomyelitis: probe-to-bone (PTB) test—1995 study by Grayson et al found that palpating
bone on probing highly correlated with presence of underlying osteomyelitis; however, recent study by Lavery et al
concluded that incidence of osteomyelitis in patients with positive PTB test much lower than originally thought; x-
rays—speaker and colleagues strongly desire x-rays as part of initial patient work-up; while not always sensitive in detecting
osteomyelitis (not visible unless bone loss 50% or more), x-rays specific when erosive and lytic changes seen on
film; radionuclide bone scans—previously thought that radionuclide bone scans always required to rule out osteomyelitis;
scan sensitive but not specific; now moving to magnetic resonance imaging (MRI; ≈90% to 100% sensitive and
80% to 100% specific for osteomyelitis); bone cultures and bone biopsies still considered gold standard for diagnosis
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| Choice of antibiotic: use flouroquinolones cautiously (known to cause emergence of resistant bacteria); new guidelines
expected on which antibiotic to use against MRSA (emergence in infectious disease community of minimum inhibitory
concentration [MIC] creep with vancomycin; ie, increasingly higher doses of vancomycin required to kill MRSA, to
point where vancomycin may no longer be drug of choice; instead, clinicians may have to use linezolid)
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| Recommended course of treatment: for mild infections in outpatients, cephalexin or amoxicillin; for deeper ulcer, add
metronidazole; if patient panallergic, penicillin; only use ciprofloxacin to treat puncture wounds that go through foot; for patients
with uncomplicated infections who get admitted to hospital, use cefazolin or clindamycin; speaker typically puts patients
on ampicillin and sulbactam (Unasyn) or piperacillin and tazobactam (Zosyn); with emerging presence of MRSA, may or may
not empirically add vancomycin (protocol to put patient in isolation until underlying bacteria identified; if patient has known
history of MRSA, may initially put him or her on vancomycin; meropenem used if patient panallergic); when culturing infection,
be sure to take culture from wound itself and not from pus
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| Experience at speaker’s institution: 7 yr ago, speaker started working as member of vascular surgery team, working
together with vascular surgeon and vascular laboratory; currently, vascular surgeons, vascular physician assistants,
vascular podiatrists, vascular technologists, and wound care nurses all in one location, down hall from both cardiology
and nephrology departments; team meets weekly with nephrologist and interventional radiologist to review all MRIs
and angiograms; colleagues from primary care, cardiology, infectious disease, and dermatology (“all the different specialists
that have anything to do with limb salvaging”) also involved; team meetings feature open dialogue as well as
educational programs “where they teach us and we teach them”; extremely successful (amputation rate decreased between
2000 and 2005, last year measured); advantage of approach that patients have to go to only one location (no
need to stand in different lines to see different specialists); patient satisfaction high
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Suggested Reading
Acosta S et al: Fatal nonocclusive mesenteric ischaemia: population-based incidence and risk factors. J Intern Med
259:305, 2006; Armstrong DG, Lipsky BA: Advances in the treatment of diabetic foot infections. Diabetes Technol
Ther 6:167, 2004; Armstrong DG, Lipsky BA: Diabetic foot infections: stepwise medical and surgical management.
Int Wound J 1:123, 2004; Atkins MD et al: Surgical revascularization versus endovascular therapy for chronic mesenteric
ischemia: a comparative experience. J Vasc Surg 45:1162, 2007; Biebl M et al: Surgical and interventional visceral
revascularization for the treatment of chronic mesenteric ischemia--when to prefer which? World J Surg 31:562,
2007; Edmonds M: Diabetic foot ulcers: practical treatment recommendations. Drugs 66:913, 2006; English WP et
al: Chronic visceral ischemia: symptom-free survival after open surgical repair. Vasc Endovascular Surg 38:493, 2004;
Faglia E et al: The role of early surgical debridement and revascularization in patients with diabetes and deep foot space
abscess: retrospective review of 106 patients with diabetes. J Foot Ankle Surg 45:220, 2006; Falkensammer J, Oldenburg
WA: Surgical and medical management of mesenteric ischemia. Curr Treat Options Cardiovasc Med 8:137,
2006; Gloviczki P, Duncan AA: Treatment of celiac artery compression syndrome: does it really exist? Perspect Vasc
Surg Endovasc Ther 19:259, 2007; Grayson ML et al: Probing to bone in infected pedal ulcers. A clinical sign of underlying
osteomyelitis in diabetic patients. JAMA 273:721, 1995; Grisham A et al: Deciphering mesenteric venous
thrombosis: imaging and treatment. Vasc Endovascular Surg 39:473, 2005; Joseph WS: Classification of diabetic foot
infections. Cutis 73(5 Suppl):20, 2004; Kansal N et al: A comparison of antegrade and retrograde mesenteric bypass.
Ann Vasc Surg 16:591, 2002; Kougias P et al: Management of chronic mesenteric ischemia. The role of endovascular
therapy. J Endovasc Ther 14:395, 2007; Lavery LA et al: Probe-to-bone test for diagnosing diabetic foot osteomyelitis:
reliable or relic? Diabetes Care 30:270, 2007; Lipsky BA et al: Diagnosis and treatment of diabetic foot infections.
Plast Reconstr Surg 117(7 Suppl):212S, 2006; Orr DW et al: Chronic mesenteric venous thrombosis: evaluation and
determinants of survival during long-term follow-up. Clin Gastroenterol Hepatol 5:80, 2007; Pinzur MS et al: Guidelines
for diabetic foot care: recommendations endorsed by the Diabetes Committee of the American Orthopaedic Foot and
Ankle Society. Foot Ankle Int 26:113, 2005; Schaefer PJ et al: Chronic mesenteric ischemia: stenting of mesenteric arteries.
Abdom Imaging 32:304, 2007; Shah BR, Hux JE: Quantifying the risk of infectious diseases for people with diabetes.
Diabetes Care 26:510, 2003; Shank CF, Feibel JB: Osteomyelitis in the diabetic foot: diagnosis and
management. Foot Ankle Clin 11:775, 2006; Sheppard SJ: Antibiotic treatment of infected diabetic foot ulcers. J
Wound Care 14:260, 2005; Sumpio BE et al: Vascular evaluation and arterial reconstruction of the diabetic foot. Clin
Podiatr Med Surg 20:689, 2003; Tentolouris N et al: Prevalence of methicillin-resistant Staphylococcus aureus in infected
and uninfected diabetic foot ulcers. Clin Microbiol Infect 12:186, 2006.
Educational Objectives
| The goal of this program is to improve the diagnosis and treatment of chronic mesenteric ischemia (CMI) and to improve
management of the infected diabetic foot. After hearing and assimilating this program, the clinician will be better able to:
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 | 1. Recognize signs and symptoms of CMI and select the best imaging test for identifying anatomic stenosis or occlusion.
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| 2. Discuss treatment modalities such as surgical bypass, endarterectomy, celiac and superior artery reimplantation, and
angioplasty and stenting, and choose the best option for each patient.
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| 3. Detect and manage unusual underlying causes of CMI, including celiac artery compression syndrome, nonocclusive mesenteric
ischemia, and mesenteric venous thrombosis.
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| 4. Describe the increased risk for infectious disease in patients with diabetes and some of the common causes of diabetic
foot problems.
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| 5. Explain the importance of early irrigation and debridement and describe the recommended course of antibiotic treatment
for diabetic foot infections.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and planning committee members
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. Kansal spoke at the 30th Annual San Diego Postgraduate Assembly in Surgery, held February 26 to March 2, 2007,
in San Diego, CA, and sponsored by the University of California, San Diego, School of Medicine, Department of Surgery.
Dr. Branks was recorded at the 3rd Annual National Surgical Symposium, held July 11-14, 2007, in Napa, CA, and sponsored
by Kaiser Permanente. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the
production of this program.
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