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
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
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
4
Q
Symptoms of AMI
A
- Generalised abdominal pain - diffuse and constant
- Out of proportion to clinical findings
- Nausea and vomitting
5
Q
Examination of AMI
A
- Non-specific tenderness
- Globalised peritonism if perforated at later stages
6
Q
Other causes of generalised abdominal pain acutely
A
- PUD
- Bowel perforation
- Symptomatic AAA
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
8
Q
Imaging for AMI
A
- CT abdomen with IV contrast
Avoid oral contrast due to difficulty assessing for bowel wall enhancement
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
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
11
Q
Definitive management options for AMI
A
- Revasculariation of bowel
- Excision of necrotic/non-viable bowel - if not suitable for revasc
12
Q
How is decision made to revascularise bowel or not?
A
- State of patient
- Bowel
- Angiographic appearance of mesenteric vessels
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
14
Q
What is short gut syndrome?
A
- Bowel is shortened
- = Cannot absorb enough nutrients from the foods you eat to maintain health
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
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
