GEMC: Mesenteric Ischemia: Resident Training

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Project: Ghana Emergency Medicine Collaborative Document Title: Mesenteric Ischemia Author(s): Andrew Barnosky, DO, MPH, University of Michigan Medical School License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/ We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. These lectures have been modified in the process of making a publicly shareable version. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact [email protected] with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit http://open.umich.edu/privacy-and-terms-use. Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers. 1

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This is a lecture by Dr. Andrew Barnosky from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.

Transcript of GEMC: Mesenteric Ischemia: Resident Training

Page 1: GEMC: Mesenteric Ischemia: Resident Training

Project: Ghana Emergency Medicine Collaborative Document Title: Mesenteric Ischemia Author(s): Andrew Barnosky, DO, MPH, University of Michigan Medical School License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/

We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. These lectures have been modified in the process of making a publicly

shareable version. The citation key on the following slide provides information about how you may share and adapt this material.

Copyright holders of content included in this material should contact [email protected] with any

questions, corrections, or clarification regarding the use of content.

For more information about how to cite these materials visit http://open.umich.edu/privacy-and-terms-use.

Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please

speak to your physician if you have questions about your medical condition.

Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers.

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Mesenteric Ischemia

Andrew Barnosky, DO, MPH Associate Professor

Department of Emergency Medicine University of Michigan Medical School

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Lecture Objectives

n To grow in our understanding of the anatomy, pathophysiology, diagnosis, and treatment of mesenteric vascular emergencies.

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Gray’s Anatomy, Wikimedia Commons

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Original Image: Gray’s Anatomy; Altered Image: Mikael Haggstrom, Wikimedia Commons

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Gray’s Anatomy, Wikimedia Commons

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Gray’s Anatomy, Wikimedia Commons

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Gray’s Anatomy, Wikimedia Commons 12

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Gray’s Anatomy, Wikimedia Commons

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Gray’s Anatomy, Wikimedia Commons 14

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Gray’s Anatomy, Wikimedia Commons

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Introduction Mesenteric Ischemia

n  A devastating disease increasing in incidence n  1/1000 hospital admissions n  2/100 hospital admissions for abdominal pain n  Despite diagnostic advances, mortality remains

approximately 70% n  Delays in diagnosis continue to decrease chance of

survival n  Presentation is nonspecific and initial abdominal

exam may be unimpressive

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History

n  1500 - First described in Florence n  1815 - Guy's Hospital, London n  1875 - Litten ligates the SMA of an animal

and records events n  1894 - Councilman describes chronic MI n  1895 - Venous thrombosis (MVT) described

by Elliott n  1959 - Non-occlusive mesenteric ischemia

(NOMI) first described in NEJM 17

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History

n  1940 - Heparin first used n  1950 - First SMA embolectomy without bowel

resection n  1958 - First successful revascularization after

SMA thrombosis n  1960 - Arteriography used successful and

became standard of diagnosis

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Anatomy

n Celiac artery - distal esophagus to second portion of duodenum

n Superior Mesenteric Artery (SMA) - duodenum to distal transverse colon

n  Inferior Mesenteric Artery (IMA) - transverse colon to rectum

n Marginal Artery of Drummond - Anastomotic collateral between SMA and IMA

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Etiology

n Acute versus Chronic n Occlusive versus Nonocclusive

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Etiology (Continued) n  50% - AMI due to an embolus to the SMA n  15% - AMI due to thrombosis of the SMA n  15% - AMI due to mesenteric venous

thrombosis n  20% - NOMI

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Superior Mesenteric Artery Embolism n  Catastrophic event typically in patients with heart disease

n  - Atrial Fibrillation n  - Arrhythmias n  - Valvular disease n  - Myocardial infarction with ventricular thrombus

n  Embolus lodges 3-10 cm distal to origin of SMA at point of taper n  - Blood flow preserved to proximal SMA branches (duodenal

and middle colic distributions) n  - Proximal small bowel and large bowel generally spared n  One-third of patients have a history of prior embolic event

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Superior Mesenteric Artery Thrombosis n Occurs in setting of long standing

atherosclerotic disease n Cause is usually rupture of a plaque at origin

of SMA n Well developed collateral may be present due

to chronicity of disease

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Mesenteric Venous Thrombosis

n Found mostly in patients with hypercoagulable states

n Half of patients have history of DVT/PE n Other predisposing factors are malignancy,

pregnancy, sepsis, portal hypertension n Presentation less acute than SMA occlusion

(i.e., harder to diagnose)

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Nonocclusive Mesenteric Ischemia (NOMI) n Occurs in low flow states (e.g., CHF, sepsis,

volume depletion) n Noted increasingly after cardiac surgery and

after dialysis n Multiple medications predispose patients n Often presents without pain, but with

distention and GI bleed n Mortality is extremely high, reflecting poor

health of population

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Chronic Mesenteric Ischemia

n  Presents as "intestinal angina“ n  Abdominal pain soon after eating, lasting 1-2 hours n  Patients develop "food fear" and "small meal

syndrome“ n  Associated weight loss n  Often concomitant atherosclerotic disease elsewhere n  Diabetes and hypertension often coexist and

predispose

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Clinical Findings History n  History is exceedingly important n  Evaluation of risk factors exceedingly important n  Classic triad -- severe abdominal pain, gut emptying,

underlying heart disease n  SMA embolus – patients may pinpoint exact moment

of pain n  SMA thrombosis – long history of intestinal angina

with escalation n  NOMI – history of low flow states

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Clinical Findings Physical Examination “In contrast to the catastrophic nature of the

pain, there is usually a paucity of physical findings. The clinician must be careful not to minimize the patient’s complaints because of lack of specific signs.”

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Clinical Findings Physical Examination n  Vital signs often normal n  Tachycardia is first finding n  Fever – elderly often do not mount this response n  Tachypnea – pain or early acidosis n  Hypothermia – may see with impending sepsis n  Hypotension – late and ominous finding n  Cold sweats – often seen as a result of overwhelming

sympathetic discharge n  Much confusion separating acute myocardial

infarction

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Clinical Findings Physical Exam - Abdomen n Often unimpressive and nonspecific n Hallmark is “pain out of proportion” n Bowel sounds are active in 3/4ths of patients

early in process (absent after complete infarction)

n  Localized tenderness rare n Peritoneal signs – late n Blood in stool - late

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Clinical Findings Physical Exam – General n Utility of the full physical exam is in the

search for other causes of symptoms n Cardiac – murmurs or arrhythmias as source

of emboli n Neuro – look for prior stroke n CHF – at risk for NOMI n Underlying malignancy – consider MVT n  “Perhaps the best overall finding was an

uneasy feeling on the part of the examining physician that his patient looks sick, but that he could not say why or from what.”

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Laboratory Studies

n There is no one test which can rule out acute MI

n Most studies lack sensitivity and specificity n Some findings may support diagnosis - but

normal values never exclude this diagnosis n Normal values (amylase) should not sway

you from pursuing the diagnosis

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Laboratory Studies n  WBC - Greater than 15,000 in 90% of patients n  Electrolytes - 50% have anion-gap metabolic acidosis with large

base deficit n  Lactate - increase in first hour and correlates with extent of

damage n  Intestinal Fatty Acid Binding Protein (IFABP)

n  Produced by enterocytes and release intestinal injury n  Half-life exceedingly short in serum n  Excreted by kidneys n  Urinary levels may prove to be valuable, but still quasi-experimental

n  EKG - Atrial fibrillation common

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Imaging Studies Plain Radiographs n  Rarely diagnostic and completely normal 25% of the

time n  Early findings nonspecific

n  Small bowel distention, air/fluid levels, ileus, etc. n  With progression of disease, ischemia leads to bowel

wall edema with "thumbprinting“ n  With necrosis, pneumatosis intestinalis, occasionally

progressing to air in the portal venous system n  Mortality is 80% if positive radiographic findings at

time of diagnosis, 30% if no abnormalities

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Imaging Studies Ultrasound n Doppler sonography may be helpful if

complete obstruction of proximal SMA n  Limited ability to detect peripherally located

emboli n Color flow duplex sonography may be good in

diagnosing chronic MI as peak systolic and diastolic velocity can be measure (not good for acute MI)

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Imaging Studies CT n All findings evident on plain x-rays can be

seen on CT as well, yet remain just as nonspecific in early disease

n CT w/IV contrast excellent in diagnosis of MVT

n CT angiography excellent in diagnosing AMI

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Imaging Studies MRI n MRI-MRA provides excellent images of

arterial and venous systems n Time required limits utility for AMI (good for

CMI) n Ability to delineate small distal emboli is

limited n Newer techniques include MRO (magnetic

resonance oximetery) n  Measures selective O2 saturation in specific

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Imaging Studies Angiography n  Remains the gold standard for diagnosing AMI n  Greater than 90% sensitivity n  Abrupt cut-off is diagnostic

n  3-10 cm distal to SMA = embolus n  Non-visualization of SMA = thrombus

n  Aggressive angiography one of few methods to decrease mortality of AMI

n  Downside: n  Invasive n  Time-consuming n  Potentially nephrotoxic

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Treatment – Overall Goals

n Reestablish blood flow as soon as possible, before irreversible bowel ischemia has occurred

n The only way to achieve this is through early diagnosis

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Treatment General Measures n  Broad spectrum antibiotics

n  Theoretical protection against bacterial translocation

n  Anticoagulation with heparin n  When to begins is controversial – discuss w/

admitting surgeon n  General

n  NG, NPO, Foley, I&O, Surgery consult n  Avoid

n  Vasoconstricting medications

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Treatment - Superior Mesenteric Artery Embolus n  Strive for immediate attempts at revascularization

n  Operative embolectomy most common with resection of areas of frank necrosis

n  If no peritoneal signs, thrombolytics may be considered n  Most often successful if embolism is only partially occluding n  If no lysis at 4 hours or peritoneal signs develop –

laparotomy indicated n  Small emboli in patients with thrombolytic hemorrhage risk

and/or poor surgical risk n  Short acting arterial vasodilator such as tolazoline

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Treatment - Superior Mesenteric Artery Thrombosis n Thrombolytics generally not successful in

long term management n Definitive revascularization recommended n Bypass grafting types:

n  Antegrade from supraceliac aorta n  Retrograde from infrarenal aorta

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Treatment - Mesenteric Venous Thrombosis n  Immediate heparin anticoagulation recommended n  Anticoagulation with coumadin for 3-6 months n  Thrombectomy if thrombus less than 3 days old n  Resection of diseased bowel as indicated n  Thrombolytics - still under study without firm

recommendation n  Thrombolytic approaches

n  Antegrade via superior mesenteric artery n  Retrograde via internal jugular vein n  Transhepatically via the portal vein

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Treatment - Nonocclusive Mesenteric Ischemia n  Surgery reserved for patients with bowel obstruction n  Discontinue alpha-agonists, digitalis, and

vasopressors n  Peripheral administration of heparin - precipitates if

given with papaverine n  Papaverine via arterial catheter during arteriography n  Consideration of revascularization n  Iloprost still under study

n  Prostacycline analog n  Fibrinolytic activity and platelet inhibitor

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Treatment - Chronic Mesenteric Ischemia n Open surgical revascularization most

common n Angioplasty with stenting for localized focal

stenotic disease

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Future Directions: Ischemia-Reperfusion Injury n  Intestinal ischemia results in formation of free

radicals n Free radicals promote systemic release of

bacterial toxins n Systemic release of toxins leads to pulmonary

complications and distant organ disease n Various medications and hyperbaric oxygen

continue being studied to limit this form of injury

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Summary

n Acute insufficiency of mesenteric arterial blood flow accounts for 60 to 70 percent of cases of mesenteric ischemia and results in mortality rates exceeding 60 percent. Specific risk factors include advanced age, atherosclerosis, low cardiac output states, cardiac arrhythmias, severe cardiac valvular disease, recent myocardial infarction, and intra-abdominal malignancy.

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Summary

n  The diagnosis of AMI depends upon a high clinical suspicion, especially in patients with known risk factors (such as atrial fibrillation, congestive heart failure, peripheral vascular disease, or a history of hypercoagulability). Rapid diagnosis is essential to prevent the catastrophic events associated with intestinal infarction. However, early signs and symptoms of mesenteric ischemia are nonspecific, and definitive diagnosis often requires invasive testing, exposing the patients who typically have several comorbidities to risk. As a result, the diagnosis is often delayed.

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Summary

n  Mesenteric angiography remains the gold standard diagnostic study for acute arterial ischemia. Early and liberal implementation of angiography has been the major factor for the decline in the mortality of patients with acute mesenteric ischemia over the past 30 years. Thus, in patients for whom a high clinical suspicion of mesenteric ischemia is present, we suggest immediate angiography rather than other imaging modalities . Such patients should also receive surgical consultation.

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Summary

n  Multidetector-row CT angiography appears to be an acceptable alternative in settings where obtaining early angiography is impractical, or there is only a moderate suspicion for acute intestinal ischemia, based upon the patient's clinical presentation. Accumulating evidence suggests that this imaging technique has a high degree of accuracy in diagnosing acute mesenteric ischemia, and it has the additional advantage of diagnosing alternative conditions.

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Summary

n The goal of treatment of patients with acute mesenteric ischemia is to restore intestinal blood flow as rapidly as possible after initial management that includes aggressive hemodynamic monitoring and support, correction of metabolic acidosis, initiation of broad spectrum antibiotics, and placement of a nasogastric tube for gastric decompression.

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“The philosophies of one age have

become the absurdities of the next, and the foolishness of yesterday has become the wisdom of tomorrow.”

William Osler 1848-1919

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