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Acute Mesenteric Ischemia and Infarction

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Acute Mesenteric Ischemia and Infarction foolad Eghbali M.D. Vascular surgeon Rasool Akram Hosp. – PowerPoint PPT presentation

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Title: Acute Mesenteric Ischemia and Infarction


1
Acute Mesenteric Ischemia and Infarction
  • foolad Eghbali M.D.
  • Vascular surgeon
  • Rasool Akram Hosp.

2
Background
  • Acute mesenteric ischemia (AMI) is a syndrome in
    which inadequate blood flow through the
    mesenteric vessels causes ischemia and eventual
    gangrene of the bowel wall.
  • Either arterial or venous disease

3
  • Arterial disease may be subdivided into
    nonocclusive mesenteric ischemia (NOMI)and
    occlusive mesenteric arterial ischemia (OMAI).
  • OMAI may be further subdivided into acute
    mesenteric arterial embolus (AMAE) and acute
    mesenteric arterial thrombosis (AMAT). Venous
    disease takes the form of mesenteric venous
    thrombosis (MVT).
  • AMI comprises 4 different primary clinical
    entities NOMI, AMAE, AMAT, and MVT.

4
  • since 1930, many advances have been made that
    allow earlier diagnosis and treatment.
  • Whereas the prognosis remains grave

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Superior Mesenteric Artery (SMA)
  • Largest caliber vessel 45-degree angle makes it
    most commonly occluded

Aorta
Celiac Trunk
SMA
IMA
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The celiac artery (CA) supplies the foregut,
hepatobiliary system, and spleen the SMA
supplies the midgut (ie, small intestine and
proximal mid colon) and the inferior mesenteric
artery (IMA) supplies the hindgut (ie, distal
colon and rectum). However, multiple anatomic
variants are observed. Venous drainage is through
the superior mesenteric vein (SMV), which joins
the splenic vein to form the portal vein
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Superior Mesenteric Artery (SMA)
  • Emboli occlude past the middle colic, causing
    small bowel ischemia

Middle Colic
SMA
Jejunal Ileal Arteries
Occlusion Point
Right Colic
Ileocolic
11
Pathophysiology
  • Insufficient perfusion of the small bowel and
    colon may result from arterial occlusion by
    embolus or thrombosis (AMAE or AMAT), thrombosis
    of the venous system (MVT), or nonocclusive
    processes such as vasospasm or low cardiac output
    (NOMI).

12
Etiologies of Acute Mesenteric Ischemia (AMI)
  • SMA Occlusion (at least 60 of cases)
  • Embolism MI, Afib, Endocarditis, Valve d.
  • Thrombosis Atherosclerosis plaque rupture
  • Nonocclusive Mesenteric Ischemia (NOMI)
  • Atherosclerosis shock vasopressors
  • Mesenteric Venous Thrombosis (MVT)
  • Primary clotting disorder

13
Etiologies of Acute Mesenteric Ischemia (AMI)
  • Focal small bowel ischemia - rare
  • Partial malrotation, volvulus, mesenteric
    hematoma, strangulated hernia
  • Unknown
  • ?Mesenteric small vessel disease

14
  • Causes of embolic AMI (AMAE) include the
    following
  • Cardiac emboli - Mural thrombus after myocardial
    infarction, auricular thrombus associated with
    mitral stenosis and atrial fibrillation, septic
    emboli from valvular endocarditis (less frequent)
  • Emboli from fragments of proximal aortic thrombus
    due to a ruptured atheromatous plaque
  • Atheromatous plaque dislodged by arterial
    catheterization

15
  • Causes of thrombotic AMI (AMAT) include the
    following
  • Atherosclerotic vascular disease (most common)
  • Aortic aneurysm
  • Aortic dissection
  • Arteritis
  • Decreased cardiac output from myocardial
    infarction or CHF (thrombotic AMI may cause acute
    decompensation)
  • Dehydration from other causes

16
  • Causes of NOMI include the following
  • Hypotension from CHF, myocardial infarction,
    sepsis, aortic insufficiency, severe liver or
    renal disease, or recent major cardiac or
    abdominal surgery
  • Vasopressive drugs
  • Ergotamines
  • Cocaine
  • Digitalis (whether digitalis use causes NOMI or
    patients who develop NOMI are older and are more
    likely to have been prescribed digitalis is
    unclear)

17
  • Causes of MVT include the following (gt80 of
    patients with MVT are found to have predisposing
    conditions)
  • Hypercoagulability from protein C and S
    deficiency, antithrombin III deficiency,
    dysfibrinogenemia, abnormal plasminogen,
    polycythemia vera (most common), thrombocytosis,
    sickle cell disease, factor V Leiden mutation,
    pregnancy, and oral contraceptive use
  • Tumor causing venous compression or
    hypercoagulability (paraneoplastic syndrome)
  • Infection, usually intra-abdominal (eg,
    appendicitis, diverticulitis, or abscess)
  • Venous congestion from cirrhosis (portal
    hypertension)
  • Venous trauma from accidents or surgery,
    especially portocaval surgery
  • Increased intra-abdominal pressure from
    pneumoperitoneum during laparoscopic surgery
  • Pancreatitis

18
Epidemiology
  • Age
  • Advanced age is a risk factor due to the
    association with atheroscleosis
  • The overall prevalence of AMI is 0.1 of all
    hospital admissions
  • No overall sex preference

19
Prognosis
  • The prognosis of AMI of any type is grave.
    Overall, the mortality rate in the last 15 years
    from all causes of AMI averages 71, with a range
    of 59-93. Once bowel wall infarction has
    occurred, the mortality rate is as high as 90.
    Even with good treatment, up to 50-80 of
    patients die.

20
History Physical
  • Classic Presentation
  • Rapid onset of severe, unrelenting periumbilical
    pain
  • Pain out of proportion to findings on physical
    examination.
  • Nausea and vomiting
  • Forceful/urgent bowel evacuation
  • Risk factors for acute mesenteric ischemia

21
History Physical
  • SMA Thrombosis
  • Prodrome of postprandial pain/nausea and weight
    loss
  • Presentation with classic symptoms
  • Non-occlusive Mesenteric Ischemia
  • Unexplained decline in clinical status or failure
    to follow expected recovery

22
History Physical
  • Mesenteric Venous Thrombosis
  • Fever
  • Abdominal distension
  • Hemoccult positive stool

23
Physical Examination
  • The different etiologies notwithstanding,
    physical examination findings are generally
    similar in patients with AMI. The main
    distinction is between early and late
    presentation. Early in the course of the disease,
    in the absence of peritonitis, physical signs are
    few and nonspecific. Tenderness is minimal to
    nonexistent. Stool may be guaiac positive.

24
  • Peritoneal signs develop late, when infarction
    with necrosis or perforation occurs. Tenderness
    becomes severe and may indicate the location of
    the infarcted bowel segment. A palpable tender
    mass may be present. Bowel sounds range from
    hyperactive to absent. Voluntary and involuntary
    guarding appears. Fever, hypotension,
    tachycardia, tachypnea, and altered mental status
    are observed. Foul breath may be noted with bowel
    infarction, from the putrefaction of undigested
    alimentary material accumulated proximal to the
    pathologic site
  • Signs reflecting risk factors for AMI may be
    noted.

25
Complications
  • Bowel necrosis necessitating bowel resection
  • Septic shock
  • Death

26
Diagnostic Considerations
  • Because acute mesenteric ischemia (AMI) is a
    condition with an unclear initial presentation,
    serious morbidity, and a high mortality rate
    without proper treatment, clinical suspicion
    should remain high. Obtain early angiography if
    any suspicion of AMI exists. Subsequent treatment
    should be initiated as rapidly as possible. No
    patient in whom AMI is suspected should be
    discharged unless AMI can be ruled out.

27
Laboratory Findings
  • Anion gap metabolic acidosis
  • Elevated arterial/venous lactate
  • Leukocytosis
  • Hemoconcentration
  • Elevated LDH, amylase, AST, and CPK
  • Elevated K and Phos are late signs

28
Radiology
  • Plain films thumbprinting, thickened bowel
    (lt40 sensitivity)
  • CT thickened/dilated bowel, intramural
    hematoma, pneumatosis (64 sensitivity)
  • MRI promising but untested to date
  • Mesenteric angiography test of choice can
    identify the type of AMI

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Differential Diagnosis
  • Other serious conditions to consider
  • Pancreatitis
  • Acute Diverticulitis
  • Acute Cholecystitis
  • Small bowel obstruction
  • Perforation of a viscous
  • Ruptured aneurysm

34
Treatment
  • Resuscitation with fluids/blood products
  • Anticoagulation, Administer heparin as a bolus of
    80 U/kg, and then as an infusion at 18 U/kg/h
    until full conversion to oral warfarin
  • Infusion of a vasodilator
  • Glucagon systemically OR
  • Papaverine through a catheter, Start an infusion
    of 30-60 mg/h after angiography,

35
  • Inpatient medications include the following
  • Papaverine - For patients with arterial occlusive
    AMI or nonocclusive mesenteric ischemia (NOMI)
  • Heparin - For patients who have mesenteric venous
    thrombosis (MVT) or have undergone
    revascularization
  • Warfarin - For long-term treatment of patients
    with MVT or atrial fibrillation
  • Broad-spectrum antibiotics and pain medications -
    For all patients
  • Thrombolytics - For selected patients with
    embolic AMI
  • Some experience with percutaneous endovascular
    interventions has been accumulated. In select
    cases, especially in isolated spontaneous
    dissection of the SMA, stent placement may offer
    the best option

36
Surgical Care
  • Before operative management of AMI, stabilize
    patients by means of intravenous (IV) fluid
    administration, antibiotic prophylaxis covering
    the colonic flora, nasogastric tube
    decompression, and bladder catheterization, with
    heparin or papaverine administered as indicated.
    Blood should be available

37
  • In all types of AMI, resection of necrotic bowel
    may be required if signs of peritonitis develop.
    Differentiation of nonviable from viable bowel
    can be enhanced by intraoperative fluorescein
    administration

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  • Thank you
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