Acute and chronic mesenteric ischaemia Flashcards

1
Q

What is AMI?

A
  • Sudden decrease in blood supply to the bowel –> ischaemia and if not treated, death
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2
Q

4 classes of AMI

A
  • Thrombus in situ - acute mesenteric arterial thrombus)
  • Embolism - acute mesenteric embolism
  • Non-occlusive - non-occlusive mesenteric ischaemia
  • Venous occlusion and congestion - mesenteric venous thrombosis
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3
Q

Cause of each class of AME

A
  • AMAT - atherosclerosis
  • AMAE - cardiac causes eg AF, post MI mural thrombi, prosthetic heart valve, thoraco-abdominal aneurysm
  • NOMI - hypovolaemic shock, cardiogenic shock
  • MVT - coagulopathy, malignancy, autoimmune disorders
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4
Q

Symptoms of AMI

A
  • Generalised abdominal pain - diffuse and constant
  • Out of proportion to clinical findings
  • Nausea and vomitting
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5
Q

Examination of AMI

A
  • Non-specific tenderness
  • Globalised peritonism if perforated at later stages
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6
Q

Other causes of generalised abdominal pain acutely

A
  • PUD
  • Bowel perforation
  • Symptomatic AAA
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7
Q

Bloods and bedside tests for AMI

A
  • ABG - assess acidosis and lactate
  • Routine bloods - FBC, U&E, clotting, amylase, LFT
  • If coeliac trunk affected, ischaemia of liver can cause deranged LFTs
  • Amylase also rises in AMI, ectopic pregnancy, bowel perf, and DKA as well as pancreatitis
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8
Q

Imaging for AMI

A
  • CT abdomen with IV contrast

Avoid oral contrast due to difficulty assessing for bowel wall enhancement

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9
Q

CT signs of AMI

A
  • Oedematous bowel - ischaemia and vasodilation
  • Then progresses to loss of bowel wall enhancement - inadequate blood flow
  • Then pneumatosis - infarction and then gas infiltration into mucosa
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10
Q

Initial management AMI

A
  • Surgical emergency = urgent resucitation and escalate to senior
  • IV fluids
  • Catheter + fluid balance chart
  • Broad spec abx - risk of faecal contamination if perforates (bacterial translocation)
  • Early ITU input - as very acidotic and high risk of organ failure
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11
Q

Definitive management options for AMI

A
  • Revasculariation of bowel
  • Excision of necrotic/non-viable bowel - if not suitable for revasc
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12
Q

How is decision made to revascularise bowel or not?

A
  • State of patient
  • Bowel
  • Angiographic appearance of mesenteric vessels
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13
Q

Management post op of excision of necrotic/non-viable bowel

A
  • ITU
  • Planned for potential re-look laparotomy in 24-48hrs
  • Majority patients end up with loop or end stoma
  • HIGH chance of short gut syndrome
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14
Q

What is short gut syndrome?

A
  • Bowel is shortened
  • = Cannot absorb enough nutrients from the foods you eat to maintain health
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15
Q

How is revasculularisation of bowel performed?

A
  • Angioplasty is preferred
  • Due to risk of aortic contamination in open surgery
  • However open embolectomy is possible through the coeliac trunk, SMA, IMA or aorta
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16
Q

Complications of AMI

A
  • Bowel necrosis and perforation
  • Mortality is high
  • Those who survive often struggle with short gut syndrome
17
Q

What is chronic mesenteric ischaemia?

A
  • Reduced blood supply to the bowel which gradually deteriorates over time
  • Due to atheroscelrosis of coeliac trunk, SMA or IMA
18
Q

Typical patient with CMI

A
  • Female
  • Over 60yrs old
  • Asymptomatic usually
19
Q

Pathophys of CMI

A
  • Gradual build up of atherosclerotic plaque
  • Narrows lumen
  • Impairs blood flow
  • = inadequate supply to bowel
20
Q

How many vessels to be affected to be symptomatic?

A
  • Due to collateral blood flow, at least two of SMA, IMA and coeliac trunk must be affected
  • Most likely with one vessel is occluded
21
Q

When can symptoms arise from CMI?

A
  • At rest, asymptomatic due to decreased demand
  • But when increased demand occurs can get symptoms eg when eating, or reduced blood volume following haemorrhage
22
Q

RF for CMI

A
  • Smoking
  • HTN
  • Diabetes mellitus
  • High cholesterol
23
Q

Symptoms if CMI becomes symptomatic

A
  • Postprandial pain - 10mins-4hrs after eating (can then develop fear of eating - sitophobia)
  • Weight loss - decreased calorie intake and malabsoprtion
  • Other vascular co-morbids eg previous MI, stroke
  • Can get changes to bowel habit (loose usually), N+V
24
Q

Examination findings CMI

A
  • Malnutrition/cachexia
  • Generalised abdominal tenderness
  • Abdominal bruits
25
Q

Differentials for non-specific abdominal pain - more chronic

A
  • Chronic pancreatitis
  • Gallstone pathology
  • PUD
  • Upper GI malignancy
26
Q

Bloods for CMI

A
  • Bloods are usually normal but routine bloods often checked
  • Electrolytes magnesium and calcium should be checked due to malnutrition
  • CV risk profile can be abnormal
  • Anaemia can make symptoms worse
27
Q

Imaging for CMI

A
  • CT angiography
28
Q

Initial management CMI

A
  • Modify RF - smoking cesssation
  • Antiplatelet and statin therapy
29
Q

Surgical options for CMI

A
  • Endovascular angioplasty + stenting
  • Open repair - endarterectomy or bypass
  • Endovascular preferred due to general nutritional status of patients and complexity of open surgery
30
Q

When is surgery management considered for CMI?

A
  • Severe disease
  • Progressive disease
  • Or debilitating symptoms eg weight loss/malabsoprtion
31
Q

How is mesenteric angioplasty performed?

A
  • Percutaneously via femoral or brachial or axillary artery
  • Cathter inserted under radiological guidance
  • When region indentified, balloon expanded to dilate vessel
  • Stenting placed to maintain vessel patency
32
Q

Risk of stenting CMI

A
  • If stent blocks - can then develop acute mesenteric ischaemia
33
Q

Complications CMI

A
  • Bowel infarction
  • Malabsorption
  • Concurrent CVD - needs managing
  • But prognosis after intervention is good
34
Q
A