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Vascular Surgery > Chap 151-154 Mesenteric > Flashcards

Chap 151-154 Mesenteric Flashcards

1
Q

In embryology, what gives rise to the abdo aorta?

A

primitive dorsal artery

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2
Q

In embryology, what gives rise to the celiac?

A

10th segmental branch

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3
Q

In embryology, what gives rise to the SMA?

A

11th segmental branch

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4
Q

In embryology, what gives rise to the IMA?

A

21st segmental branch

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5
Q

What are the branches of the celiac?

A

left gastric
splenic
common hepatic

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6
Q

What is the most frequent anatomic variation of the celiac?

A

hepatic arises from SMA or directly from aorta

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7
Q

What are the branches of the SMA?

A 
PDA
middle colic
right colic
ilieocolic
third order branches
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8
Q

What are the branches of the IMA?

A 
sigmoidal branches
left colic (becomes marginal artery)
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9
Q

What are SMA and IMA connections?

A

marginal artery
meandering artery
sigmoidal branches lead to L and R rectal arteries which collateralize with branches of hypogastric

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10
Q

What are SMA and IMA connections?

A 
marginal artery 
meandering artery (l colic to middle colic)
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11
Q

How does percentage of blood flow in the bowels change with eating?

A

10% of CO with shock
25% at rest
35% after large meal

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12
Q

What do waveforms of the SMA look like during fasting and postprandial?

A

high arterial resistance with low diastolic flow

low-resistnace throughout both systole and diastole

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13
Q

What is NOMI?

A

Impaired intestinal perfusion in absence of thromboembolic occlusion
10% of mesenteric ischemia

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14
Q

What causes NOMI?

A

vasospams in arteries that supply mucosal and submucosal layers in SMA distribution

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15
Q

What are angiogrpahic findings for NOMI?

A

Narrowing of the origins of multiple branches of SMA Alternate dilation and narrowing of intestinal branches (string of sausages)
Spasm of mesenteric arcades
Impaired filling of the intramural vessels.

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16
Q

What are RF for NOMI?

A 
low flow states
hypovolemia
systemic vasoconstrictirs
AI
CPB
reperfusion injury
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17
Q

What is treatment for NOMI?

A

IA infusion of vasodilator (mort 50%)
Papverine at 30-60mg/hr
Papaverine metabolized by the liver so hypotension rarely a problem

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18
Q

What are celiac-sma collaterals?

A

GDA-PDA

19
Q

What are IMA-internal collaterals?

A

hemorrhoidals to internal iliac

20
Q

What are causes of visceral vessel disease?

A 
Atherosclerosis most common
Fibromuscular disease
Dissection, 
neurofibromatosis
Rheumatoid arthritis
Takayasu arteritis
Giant cell arteritis
Polarteritis nodosa
Radiation injury
Systemic lupus
Buegers disease
Drugs like cocaine
Median arcuate ligament syndrome
21
Q

What is natural history of visceral vessel stenosis?

A

1/3 devel mesenteric schema within 3 years

largely asympto until at least two vessels with critical stenosis

22
Q

What is clinical presentation for CMI?

A

Food aversion
Postprandial pain 30 mins after a meal persisting for 5-6hours
Midabdo in location and crampy or dull
WL

23
Q

What velocities on duplex suggest stenosis?

A

> 70%
ESV SMA >275
ESV celiac >200

> 50%
SMA EDV>45
celiac EDV >55 or reversal hepatic flow

24
Q

What are other diagnostic test?

A

CTA/MRA

gastric tonometry

25
Q

What are positive result of gastric tonometry for CMI?

A

Reduced CO2 washout from ischemic tissue cause PCO2 to rise

26
Q

What are positive result of gastric tonometry for CMI?

A

Reduced CO2 washout from ischemic tissue cause PCO2 to rise

27
Q

What are indication for revasc for CMI?

A

symptoms
some suggest 3 VD
during aortic reconstruction

28
Q

What is advantages of endovascular?

A

likley shorter hospital stays, reduced M&M

probably less long-term patency

29
Q

What are open bypass strategies?

A

supracelia (tunnel retropancreatic, ant to L renal

retrograde from infrarenal aorta or CIA (right lays better)

30
Q 
What are the results of open vs endo
symptom relief?
survival?
M&M?
restenosis rate?
A

same 90% for both
60% 5 year survival
endo lower M&M
endo higher restenosis

31
Q

What are open bypass strategies?

A

supracelia (tunnel retropancreatic, ant to L renal

retrograde from infrarenal aorta or CIA (right lays better)

32
Q

What is median arcuate ligament syndrome?

A

Fibrous edge of diaphragmatic crura croseses ant to aorta and above celiac and compresses celiac

33
Q

What is treatment for MALS?

A

division of crura with endo possibly

34
Q

What are features of embolism in acute mesenteric ischemia?

A

50% of cases
50% lodge distal to middle colic
25% are thrombosis on top of chronic disease

35
Q

What are features of AMI on X-ray?

A

Thumbprinting in advanced cases of ischemia (pneumatosis)

36
Q

What are features of AMI on CT?

A 
Pneumatosis
Vessel occlusion
Hepatic venous air
Lack of bowel wall enhancement
Free ait
Solid organ infarct
Mucosal enhacement
Ascites
37
Q

What are techniques to examine the bowel intra-operatively?

A 
visible/palpable pulsation in arcade
doopler signals in the arcade
color and appearance of the bowel serosa
peristalsis
bleeding from cut surfaces
fluorescein 
perfusion fluorometer  
laser Doppler flowmeter
38
Q

What are causes of mesenteric vein thrombosis?

A 
idopathic (primary)
trauma
inflam state (pancreatitis)
peritonitis
portal htn
obesity
hypersplenism
thrombophilia
39
Q

What does bowel look like on inspection?

A

limited segment of intestinal schema with edema and reddish discolouration
small bowel and mesentery

40
Q

What does bowel look like on inspection?

A

limited segment of intestinal schema with edema and reddish discolouration
small bowel and mesentery

41
Q

What are treatment options?

A

if no peritonitis then AC with heparin

if peritonitis or bleeding, the ex lap, bowel resection

42
Q

What is in hospital mortality for MVT?

A

20%

43
Q

What are other therapeutic options for MVT?

A

TIPS
perc transhepatic tpa
thrombolysis via SMA

Vascular Surgery (53 decks)

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