1.12 Mesenteric Ischemia Flashcards

1
Q

Describe the three major vascular trunks arise from the aorta to supply the intestines.

A

o Celiac axis: supplies oxygenated blood to the foregut which includes portions of the liver, spleen, gallbladder, pancreas, esophagus, and stomach.

o Superior mesenteric artery (SMA): delivers blood to the small intestine (distal duodenum extending to the appendix), in addition to the ascending and proximal transverse colon.

o Inferior mesenteric artery (IMA): distributes blood to the distal portion of transverse colon, the descending colon, and the rectum.

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2
Q

Your patient is suffering from mesenteric ischemia. In broad terms, what causes this, how is it categorized?

A
  • Results from decreased blood flow
    • Hypoperfusion: shock, vasospasm, or vascular occlusion
  • Categorized as either acute or chronic based on how quickly the condition develops
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3
Q

Your patient has acute mesenteric ischemia (AMI). Why is mortality rate 40-70%?

What circumstance leads to 70% fatality?

Describe the causes of Occlusive AMI versus Non-Occlusive AMI.

Describe Mesenteric Venous Thrombosis specifically.

A
  • AMI
    • 40-70% mortality due to necrosis, perforation, and sepsis
    • 70% fatality if diagnoses > 24h after onset
  • Occlusive AMI
    • Causes
      • 50% caused by SMA embolus (i.e. a fib, endocarditis)
      • 15-25% of cases caused by arterial thrombosis (i.e. CHF, PAD, CAD)
      • Vasospasm in intestinal vessels
      • Mesenteric vessel occlusion due to intestinal torsion from strangulated hernia or volvulus
  • Non-Occlusive AMI
    • Lead to: bowel ischemia or infarction due to decreased mesenteric blood flow
    • Causes
      • Low CO
      • Hotn (MAP < 45)
      • Shock causes non-occlusive vasoconstriction of the splanchnic vasculature (liver, pancreas, spleen, gut circulation)
        • Small intestine can compensate for decreases in up to 75% of blood flow, but only for a max of 12h
      • Vasopressors, esp at max doses
    • Mesenteric Venous Thrombosis
      • Less common (15-25%)
      • Causes
        • Hypercoagulability, abd trauma, intra-abdominal hypertension, vasculitis, pancreatitis, cirrhosis, IBD
        • Intravascular volume loss d/t surgery, intra-abdominal infections, oral contraceptives, smoking
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4
Q

Describe your patient’s classic AMI presentation.

How about abd exam?

A
  • AMI Presentation:
    • Sudden onset of severe abdominal pain
    • Pain is out of proportion to the patient’s abdominal exam
    • Pain is typically periumbilical area or epigastrium.
  • Abdominal exam:
    • Diffuse, non-specific tenderness without peritoneal signs such as guarding or rebound tenderness.
    • GI bleeding occurs late in the disease process
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5
Q

Your patient with AMI commonly has involvement of which regions of the mesenteric vasculature?

Describe the patho and potential impact

A
  • Location(s) of ischemia:
    • Commonly, “watershed” regions are involved.
    • Watershed regions are supplied by the distal ends of two major arteries.
    • The rectum, rectosigmoid junction, splenic flexure, and left colon, which are supplied by both the SMA and IMA.
  • During hypovolemia or hypoperfusion, watershed areas are susceptible to ischemia
  • The abrupt decrease in blood flow to these portions of the large intestine leads to abdominal pain, which may be located in the left side
  • If the entire thickness of the bowel wall is involved, bowel perforation and peritonitis can occur
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6
Q

Your patient with chronic mesenteric ischemia is likely to have what risk factors?

What portion of the bowel is usually affected?

What is the patho/progression of the disease?

When do symptoms usually occur, and what are the symptoms?

A
  • Patients with CMI typically have wide-spread atherosclerotic disease, including CAD
    • Risk factors include: Smoking, DM, HTN, and HLD
  • CMI typically affects the small intestine
  • Patho/progression:
    • Inflammation occurs over a period of time
    • Collateral circulation develops
    • Symptoms occur when two of the three major arteries are affected
  • Symptoms
    • Symptoms occur gradually and may include abdominal pain, nausea, vomiting, and may progress to gastrointestinal bleeding
    • Pain after eating (typical onset is between 10-180 minutes after eating), due to the need for increased post-prandial intestinal blood flow
    • Pain can lead to fear of eating (sitophobia) and weight loss.
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7
Q

Describe your diagnostic process for mesenteric ischemia.

What should give you a particularly high index of suspicion?

Labs?

Lab findings?

Imaging?

Imaging findings?

A
  • Diagnosis
    • Mesenteric ischemia is often a diagnosis of exclusion
    • Early diagnosis and intervention decrease mortality.
    • Have a high index of suspicion of AMI in patients with acute abdominal pain out of proportion to exam findings, especially those over age 60 with a history of vascular disease
      • Some may have abdominal bruits
      • Some may have decreased lower extremity hair growth
      • May have weak peripheral pulses
  • Lab tests:
    • BMP, lactic acid, LFTs, CBC, PT, aPTT, LDH, and stool guiac
    • Leukocytosis, metabolic acidosis, and elevated lactic acid levels are common as AMI progresses
    • These lab values may be normal early in the course of AMI
  • Imaging:
    • Biphasic CTA (CT angiography) abdomen & pelvis with and without IV contrast is the most common test for definitive diagnosis
      • Benefits: Non-invasive and are able to evaluate for multiple causes of abdominal pain and leukocytosis compared to angiography
      • Non-contrasted scan allows for visualization of arterial calcification
      • Arterial and venous phases (biphasic) help determine the presence of arterial and venous thrombosis
      • CTA is 96% sensitive and 94% specific for detecting mesenteric ischemia
      • Oral contrast is not needed to diagnose intestinal ischemia
      • Findings
        • CT scans can assess for bowel wall edema or intramural hemorrhage
        • Reperfusion events are associated with bowel wall thickening and mesenteric fat stranding on CT
        • Free fluid within the abdominal cavity is commonly found in patients with non-occlusive AMI
        • Free air is an uncommon finding
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8
Q

Describe your initial treatment for acute mesenteric ischemia

A
  • NPO, bowel rest initiated, nasogastric decompression
  • Medical therapy includes smoking cessation, control of HTN, and administering statins and aspirin
  • Goal is to restore adequate organ perfusion
    • Isotonic IV fluids helps prevent worsening ischemia.
    • If possible, avoid using vasoconstrictor agents to increase BP since they may worsen AMI due to decreased mesenteric blood flow.
    • Inotropic therapy may improve hemodynamics by increasing stroke volume (SV) and cardiac output (CO).
    • Broad-spectrum antibiotics (gram negative & anaerobic coverage) are indicated in patients with evidence of AMI due to the risk of necrotic bowel perforation and peritoneal contamination
    • IV analgesia.
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9
Q

Describe definitive treatment for mesenteric ischemia

A
  • Medical therapy is commonly used for non-occlusive disease
    • Continuously infusing nitroglycerin, or other parenteral vasodilators may augment blood flow
    • Continuous infusions of papaverine are administered into the mesenteric arteries with intra-arterial catheters placed during angiography to improve circulation to the gut
      • Papaverine decreases arterial spasms, allowing for improved blood flow
  • Patients without perforation or any absolute contraindications
    • Administering thrombolytics within eight hours of the onset of abdominal pain may restore blood flow
  • Patients with acute occlusion who present with acute abdominal pain, signs of peritoneal irritation, evidence of necrosis, and/or clinical deterioration
    • Should have exploratory laparotomy with surgical embolectomy and/or bowel resection may be necessary depending on size of the clot(s) and the extent of the intestinal ischemia
  • Post-operatively
    • Patients are anticoagulated with either low-molecular weight (LMWH) or unfractionated heparin (UFH)
    • Hypercoagulable patients may require life-long oral anticoagulation
    • Patients with CMI can undergo angioplasty and stenting of the affected artery
    • Signs of stent restenosis are similar to those patients have pre-treatment, including post-prandial pain
    • Post-operatively, patients are at risk for bleeding, infection, deep venous thrombosis (DVT), and protracted ileus
    • Patients who are post-bowel resection for AMI may require long-term parenteral nutrition (PN)
    • Patients who have had significant amounts of bowel resected are at risk for diarrhea and malabsorption of nutrients.
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