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Vascular Surgery > Renal and Mesenteric > Flashcards

Renal and Mesenteric Flashcards

1
Q

Clinical Criteria for Renal Vascular Hypertension and Ischemic Nephropathy

A

Clinical Criteria for Renal Vascular Hypertension and Ischemic Nephropathy

Clinical Criteria for Diagnosis of Renal Vascular Hypertension

Recent onset

Resistant to drug treatment (difficult to control)

Retinopathy and end organ damage greater than for equivalent essential hypertension

Kidney dysfunction

Recurrent flash pulmonary edema

Continuous abdominal bruit

History of smoking

Other vascular disease

Clinical Criteria for Diagnosis of Ischemic Nephropathy

No intrinsic kidney disease

Recent-onset azotemia

Progressive azotemia

Hypertension

Other vascular disease

Smoking

Unequal kidney size

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2
Q

Anatomic Criteria for Diagnosis of Hemodynamically Significant Renal Artery Stenosis

A

Stenosis ≥70% diameter (∼85% cross-sectional area)

Post-stenotic dilatation

Collateral circulation

Reduced kidney size
•

Absolute length discrepancy ≥1.5 cm
•

Documented length decrease ≥1cm

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3
Q

Criteria for Renal Artery Intervention

A

Criteria for Intervention
Clinical Criteria for Ischemic Nephropathy and Renal Vascular Hypertension

Chronic progressive renal insufficiency: SCr ≥2.7 mg/dL

Drug resistance (five medications) and accelerated hypertension

Anatomic Criteria (by MRA and DSA) for Hemodynamically Significant Renal Artery Stenosis

≥80% right renal artery stenosis

≥90% left renal artery stenosis

Atrophic left kidney

Physiologic Criterion (Selective Right Renal Artery and Aortic Pressure Measurements) for Hemodynamically Significant Renal Artery Stenosis

≥25% mean arterial right renal artery pressure gradient

DSA, Digital subtraction angiography; MRA, magnetic resonance arteriography; SCr, serum creatinine.

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4
Q

Factor most important in predicting preservation of renal function

A

GFR

Those data that do show a benefit in preserving renal function also show that the groups most likely to benefit from intervention are those with stages 3A and 3B dysfunction (GFR 45-59 and 30-44). Those presenting with lower GFRs tended to progress to end-stage renal disease regardless of treatment, suggesting that the kidney is already injured beyond the point of retrieval. The degree of renal artery stenosis, patient age, preprocedural blood pressure control or number of required antihypertensive medications have not been shown to directly play a role in determining appropriate patients for intervention.

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5
Q

First line therapy fro treatment of renal FMD

A

Balloon angioplasty alone is considered to be the first line approach to renal FMD.

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6
Q

Indications for renal artery aneurysm intervention

A
  • 3cm
  • symptomatic
  • All sizes in:
  • women of child bearing age
  • refractory HTN and renal artery stenosis
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7
Q

Diagnosis of renal vein thrombosis

A

CTV

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8
Q

Treatment of renal vein thrombosis

A

The treatment of renal vein thrombosis is initially anticoagulation. Unfractionated heparin followed by warfarin therapy has long been the standard. Treatment lengths vary but generally a 6-month course of anticoagulation is recommended. Thrombectomy (catheter-directed or open) or thrombolysis should be reserved for select situations, such as a threatened kidney in a young patient with acute renal failure, failure or complication of oral anticoagulation, or thrombosis of a solitary kidney with associated acute renal failure. Nephrectomy is reserved for cases of post-infarction hemorrhage. Thrombolysis typically requires both venous and arterial access. The venous access is to lyse the main renal vein and its branches, whereas the arterial catheter to drip thrombolysis agents into the renal parenchyma to clear intra-parenchymal thrombus.

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9
Q

Management of renal artery dissection

A

Spontaneous isolated renal artery dissection is rare and only represents one fourth of all renal artery dissections. There is predominance in males of 4:1. The mean age is 40 to 50 years. The presence of hypertension suggests renal ischemia and the presence of flank pain, hematuria and proteinuria suggests renal infarction. The extent of the dissection determines the optimal treatment approach. Endovascular treatment is avoided when there is branch involvement, but may be performed for focal main renal artery dissections. Renal artery bypass is utilized when there is a chance to salvage the kidney. Approaches such as in-situ repair, auto-transplantation and ex-vivo surgery may be performed for renal branch involvement. Nephrectomy is required when there is uncontrolled hypertension in the setting of irreversible renal ischemia and extensive dissection into the renal artery branches.

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10
Q

Narrowed Aorto-mesenteric angle is found in?

A

Discussion

The patient’s symptoms of painless bilious emesis after an episode of weight loss are consistent with superior mesenteric artery (SMA) syndrome. SMA syndrome tends to affect young women with a lean body type between the ages of 10 and 39 years of age. The SMA branches from the aorta at an acute angle behind the pancreas. The aorto-mesenteric space contains retroperitoneal fat, the uncinate process of the pancreas, lymphatics, third portion of duodenum and left renal vein. The adipose tissue is felt to displace the SMA anteriorly to allow for the duodenum to cross through the window without extrinsic compression. Episodes of significant weight loss are felt to reduce the adipose tissue in this space resulting in a reduction of the aorto-mesenteric angle that results in the SMA compressing on the third portion of the duodenum causing a functional obstruction. Stenosis of the SMA might result in mesenteric ischemia which is typically painful and does not improve with jejunal feeding. The celiac artery with the configuration of the J-hook is consistent with celiac artery compression; however, the hallmark of the median arcuate ligament syndrome, the clinical syndrome associated with celiac artery compression is post-prandial abdominal pain. The patient in question has painless emesis. The replaced right hepatic artery is merely an anatomic variant of the mesenteric anatomy that is important to know, but does not typically result in symptoms. Left renal vein stenosis can occur in this setting, however, patients tend to present with flank pain and hematuria.

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11
Q

Treatment of mesenteric vasospasm?

A

Vasospasm in the distribution of the SMA is the cause of nonocclusive mesenteric ischemia (NOMI). The excessive sympathetic activity that occurs during cardiogenic shock or hypovolemia, helps to maintain cardiac and cerebral perfusion at the expense of mesenteric blood flow. The treatment of NOMI is supportive therapies aimed at improving volume status and cardiac output. In some cases, intra-arterial infusion of vasodilators, especially the phosphodiesterase inhibitor papaverine at a dose of 30 to 60 mg/h, into the SMA may be employed. Operative exploration may be required if peritonitis ensues, as this may indicate presence of gangrenous bowel requiring resection.

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12
Q

Duplex criteria for mesenteric artery stenosis

A

The criteria of a PSV of greater than 200 cm/sec in the celiac artery and greater than 275 cm/sec in the superior mesenteric artery are the most accurate criteria to indicate a stenosis of 70% or greater, with a 92% sensitivity and 96% specificity as well a positive predictive value of 80% and a negative predictive value of 99%. The Bowersox criteria uses an EDV of 45cm/sec or greater to identify a stenosis in the superior mesenteric artery of more than 50%. This has a 91% specificity and 90% positive predictive value. For the celiac artery, reversed flow in the branched arteries is diagnostic of occlusion In combination with an elevated PSV in the superior mesenteric artery in a patient with abdominal pain, the diagnosis of chronic mesenteric ischemia should be considered.

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13
Q

How many patients have bilateral RAS? Have complete occlusion?

A

12%
12%

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14
Q

What is the natural hx of RAS?

A

3 years
about 8% of normal and 40% subcritical blockage progress to >60% stenosis

7% of >60% progressed to occluded

>60% will have decline in renal function, decrease renal size
10% progress to dialysis in 4 years

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15
Q

What factors are associated with progression?

A

age, high SBP, smoking, female, poorly controlled HTN

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16
Q

What is the pathogenesis of RAS?

A

athero 80%
FMD 15%
dissection 1%

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17
Q

How dose RAS cause HTN?

A

renal blood flow reduced, juxtaglomerular cells convert prorenin into renin and secrete into circulation.

renin converts angiotensinogen to angiotensin I then to angiotensis II by ACE.

AII causes blood vessel constriction and HTN. also secretes aldosterone which causes renal tubules to reabsorb NA and water into the blood (volume expansion).

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18
Q

What are the clinical presentations of RAS?

A

50% have no symptoms
ARF when starting ACEi if bilat RAS
HTN crisis
flash pulmonary edema

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19
Q

What blood work can support RAS?

A

urea and cr may be elevated
strain pattern on EKG
LVH
elevated plasmin renin

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20
Q

What findings on duplex can support RAS?

A

critical stenosis = peak systolic velocity in main RA >1.8-2.9 m/sec with post stenotic turbulence >60%

ratio renal artery to aortic peak systolic >3.5 =60%

blunted waveforms with delayed systolic upstroke are indicative of a proximal stenosis

acceleration time >100msec indicates critical stenosis within prox renal artery

resistive index
peak sys gel-end diastolic velocity/peak sys vel
>0.8 may be critical RAS

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21
Q

what is medical management in RAS?

A

ACEi-first line/ARB
then CCB/BB
statin (decrease risk of progression)
RF modification

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22
Q

What are indications for revascularization if RAS asymptomatic? (AHA)

A

IIb percutaneous
if bilat or solitary kidney and hemo signify RAS

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23
Q

What are indications for revasc in HTN? (AHA)

A

IIa
perc
hemo signif RAS, accelerated HTN, resistant HTN, malignant HTN, unexplained unilateral kidney and HTN with med intolerance

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24
Q

What are indications for revasc in renal dysfunction? (AHA)

A

IIa
progressive kidney disease and bilat or solitary kidney
IIB
chronic renal insuff and unilat RAS

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25
Q

What are indications for revasc in CHF/angina? (AHA)

A

I
percutaneous with RAS and recurrent unexplained CHF or sudden unexplained pulmonary edema
IIA
RAS and unstable angina

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26
Q

What do you consider open surgery?

A

not amenable to endovascular
early branching, segmental arteries
patient needs pararenal reconstruction
failed endo esp FMD

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27
Q

During open bypass what adjuncts can be administered/done to protect kidney?

A

mannitol 12.5 mg early in operation
repeat dose before and after ischemia 1g/kg
mannitol increase GFR and renal plasma flow without increase in blood volume

intermittent perfusion
cold perfusate
slush/ice

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28
Q

Who benefits most from interventions?

A

with rapid decline in prep GFR with severe bilat RAS and severe HTN

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29
Q

During open bypass what adjuncts can be administered/done to protect kidney?

A

mannitol 12.5 mg early in operation
repeat dose before and after schema 1g/kg
mannitol increase GFR and renal plasma flow without increase in blood volume

intermittent perfusion
cold perfusate
slush/ice

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30
Q

what is treatment for renal vein thrombosis? when to consider sx?

A

3-6 months of anticoagulation
thrombectomy reserved for bilat thrombosis, PE, single kidney, caval thrombosis, ARF, persistent serve symptoms, CI to AC

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31
Q

What are result for open repair for RAS?

A

patency for bypass at 3 years 97%
85% improvement of HTN (variable)
3.3% re-stenosis
declinig renal function 4%
morbidity 10-20%
mortality 5%
70% removed from dialysis

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32
Q

For acute renal ischemia, how long before irreversible ischemia?

A

1 hour 70-80% can recover with weeks
3-4 hours irreversible

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33
Q

What are consequences of thromboses renal vein?

A

acute renal ischemia from
congestion and edema

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34
Q

what are the symptoms of renal vein thrombosis?

A

capsular distention leading to pain
triad, flank pain, hematuria, thrombocytopenia (13%)

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35
Q

what is treatment for renal vein thrombosis? when to consider sx?

A

3-6 months of anticoagulation
thrombectomy reserved for bilat thrombosis, PE, single kidney, cabal thrombosis, ARF, persistent serve symptoms, CI to AC

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36
Q

What is treatment for RA embolism or thrombosis?

A

AC alone unless bilat or solitary kidney

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37
Q

What are the results of AC for RA thrombosis? for OR?

A

1 month mort 10%
60% normal renal function at long-ten follow-up
8% required dialysis

25% mortality with open

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38
Q

What is middle aortic syndrome?

A

coarctation of the abdominal aorta

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39
Q

What causes middle aortic syndrome?

A

over fusion of the two dorsal aortas during 4th week of gestation

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40
Q

What disease associated with MAS?

A

NF-1
williams syndrom
maternal rubella
takayasu
umbilical artery catheterization

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41
Q

What stenosis are associated with MAS?

A

splanchnic 90%
RA 60%

usually ostial

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42
Q

What are clinical features of MAS?

A

HTN (HA, seizure, AKI, bell’s palsy,)
lower extremity fatigue (uncommon)
FTT
intestinal angina
LVH, flash PE,

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43
Q

What is the definition of HTN in children?

A

SBP or DBP >95th percentile for sex age and hgt

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44
Q

What is management of MAS?

A

anti htn
patch angioplasty
reimplant viscerals
thoracoabdominal bypass

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45
Q

What sized graft to use for TA bypass for children, adolescents and adults?

A

8-12mm children
12-16 early adolescents
14-20 late adol, adults

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46
Q

whats the repp rate at 5-10years?

A

10%
axial growth not significant after10 yo

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47
Q

What is the usual appearance/location of RA aneurysms?

A

true
90% extraparenchymal
75% saccular
usually at main renal artery bifurcation

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48
Q

What are causes of RAA?

A

FMD
EDS
dissections
iatrogenic
trauma
post-stenotic dilation
polyarteritis nodosa (intrarenal)

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49
Q

what is presentation of RAA?

A

asympto
1/3 with symptoms
HTN, flank pain, hematuria, rupture
RI with distal emboli or compression

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50
Q

What are indications for intervention?

A

>2-3cm
rupture (10% mortality)
consider if pregnant
HTN—DBP >90 despite 3 anti-HTN
Dissection if viability threatened

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51
Q

What is mortality and patency of open repair?

A

1.7%
96% 4 year patency

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52
Q

What are components of cold perfusion preservation solution?

A

KCL, NA, phosphate, Bicarb, chloride

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53
Q

what is polyarteritis nodosa?

A

medium sized arterial vessel vasculopathy that cause small aneurysms that are strung like beads (rosary sign)

tx cyclophosphamide and steroids

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54
Q

What is the presentation of renal AVM?

A

hematuria (70%)
HTN
RI
high output CHF,
rupture
vague abdo/flank pain

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55
Q

Which more common r or l?

A

right

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56
Q

what are causes of renal AVM?

A

congenital
acquired (biopsy 1-10% incidence, trauma, iaotro)
FMD
aneurysm/malignancy erosion
nephrectomy

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57
Q

What is appearance of renal AVM on CT?

A

filling defect in kidney with dilated vessels

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58
Q

When to tx? and what tx?

A

after bx most close spon within one year
most don’t require tx
consider if HTN

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59
Q

What is difference in pathophys in bilateral and unilateral RAS and RV-HTN?

A

Juxtaglomerular cells release rennin—angiotensinogen to AI, ACE then cleaves to AII.
AII causes vasoconctriction and stimulates reabsorption of NA and H2O
Angio recep type I activation leads to hyperplastic remodeling of wall of periph arteries and arterioles
AII promotes volume expansion by activating ATR1 on renal tubules wo increase NA reabs and stimulating release of aldosterone (promotes renal tubular NA reabsorp)
In paient with one functional kidney, this volume expansion can be blunted
In bilat RAS or solitary kidney cannot compensate and result in Goldblatt volume dependent HTN

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60
Q

what are clinical characteristics of RV-HTN?

A

Bilat RAS may present with acute RF with ACEi trial (increased efferent arteriolar tone from AII critical compensation mechanism to maintain filtration pressure)

Flash pulmonary edema/CHF

Recalcitrant HTN previously well controlled

Slowly increasing serum
cr levels

Unprovoked hypoK

Abrupt onset of HTN

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61
Q

list causes of RV-HTN. which are 3 most common?

A

RAS
FMD
dissection

Takayasu (sub-continent and far east

hypoplastic/MAS in children
Emboli
Trauma
Ligation during surgery
Extrinsic compression

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62
Q

How does captorpil renogram work? what abnormal/normal rest?

A

Captopril ACEi
In reduced perfusion, kidney respond with efferent arteriole constriction caused by AII. If this is blocked then decline in renal function due to loss of compensatory efferent arteriolar contriction.
If contra kidney normal will show enhanced excretory functio after ACEi and efferent arteriolar dilation leads to increase GFR in setting of normal perfusion.

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63
Q

What are signs/symptoms of RV-HTN?

A

Bilat RAS may present with acute RF with ACEi trial (increased efferent arteriolar tone from AII critical compensation mechanism to maintain filtration pressure)

Flash pulmonary edema/CHF

Recalcitrant HTN previously well controlled

Slowly increasing serum cr levels

Abdominal bruit

64
Q

What are RF for contrast-induced nephrotoxicity?

A

Age
CKD
Diabetes mellitus
Hypertension
Metabolic syndrome
Anemia
Multiple myeloma
Hypoalbuminemia
Renal transplant
Hypovolemia and decreased effective circulating volumes
Urgent
Volume of contrast

65
Q 
# Define resistive index? 
how do yo calculate? 
What are normal values?
A

Sonographic index used to asses for renal arterial disease

(Peak systolic velocity-end diastolic velocity)/peak systolic velocity

Normal 0.7
>0.8 may be critical RAS but not specific for stenosis

66
Q

What are the mechanisms by which AII causes HTN?

A

vasoconstriction

increase renal tubular cell absorption of sodium

release of aldosterone which promotes renal tubular sodium absorption

acts on nuclei of the brain responsible for BP regulation (stimulates thirst)

67
Q

What are the effects on the unaffected kidney in RAS?

A

exposure to sustained HTN and circulating ATII and aldosterone
efferent and afferent arteriolar vasoc
sustained decrease in glomerular filtration
afferent arteriolar hypertrophy and arteriosclerosis

68
Q

How does renal vein renin assays work?

A

stop antiHTN
give lasix night before
catheter in each renal vein and one in IVC
reference sample then samples q5mins x2

69
Q

What are abnormal values for renal vein renin assay?

A

renal vein to systemic ration
>1.5 is positive

70
Q

What is the difference in stenting vs surgery for RAS

A

MA
BP control equivalent

71
Q

Who to treat for RAS?

A

uni-if severe HTN and low risk
bilat but one kidney sever-treat like uni disease
bilat severe-htn severe and renal dysfunction

72
Q

What are open techniques for RAS?

A

aorto renal bypass
thromboendarterrectomy
renal artery reimplantation

hepatorenal bypass
splenorenal bypass
ex vivo reconstruction

73
Q

What are the results of the CORAL trial?

A

stenting showed no benefit over PMT in reducing death or MACE in RAS
STAR and ASTRAL trial demonstrated the same

74
Q

What are components of cold perfusion preservation solution?

A

K
sodium
phosphate
chloride
bicarb

75
Q

What is a cortical rim sign?

A

on CTA the cortical rim is capsular perfusion from collaterals

76
Q

What are catheters that can be used to select the renals?

A

KMP
Sos Omni
C1, C2
shepherd hook
simmons
JB1

77
Q

What are endovascular treatments for RA embolism?

A

CDT
aspiration
covered stent

78
Q

Which RA embolism to offer intervention?

A

acute and potentially salvageable renal function esp. bilateral embolism

79
Q

What is the mortality of surgical management for RA embolism?

A

25%

80
Q

How is the management of RA thrombosis different to Renal artery embolism?

A

Will need angioplasty and stenting
need bypass or endart

81
Q

What is the natural history of acute arterial renal ischemia?

A

glomerular collapse and tubular necrosis
1hour warm–70% loss of Renal function that can recover within weeks
3-4hours irreversible ischemia

82
Q

What are the symptoms of renal vein thrombosis?

A

edema causes capsular distention which causes back/abdo pain
hematuria
anuria
acute HTN

83
Q

What is the classic triad for renal vein thrombosis?

A

flank mass
gross hematuria
thrombocytopenia
15%

84
Q

What is the most common causes for renal vein thrombosis?

A

malignancy
nephritic syndrome

85
Q

How do you treat renal vein thrombosis?

A

anticoagulation

86
Q

What is management of RA embolism?

A

unilateral–anticoagulation
80% success, 8% require dialysis

87
Q

What is the risk of surgical management of RA thrombosis?

A

25% mortality

88
Q

When to treat renavascular trauma?

A

bilateral injury
solitary kidney

89
Q

What are treatment options for renavascular trauma?

A

Nephrectomy, embolization, bypass, endovascular
majority non-op

90
Q

what is middle aortic syndrome?

A

abdo aortic coarctation and hypoplasia

91
Q

Where is MAS most often located

A

suprarenal then infra

92
Q

What are associated disorders with MAS?

A

Neurofibromatosis-1, (25% of abdo ao coarc have NF-1
Williams syndrom, alagille syndomr
Maternal rubella
Takayasu (more likely arch or DTA
Umbilical artery catheterization

93
Q

What vessels have associated stenosis?

A

Splanchnic 87%
RA 62%
Usually ostial

94
Q

what are symptoms of MAS?

A

Lower extremity fatigue is infrequent
Intestinal angina 6%
Food aversion, weight loss
HTN
HA, seizure, epistaxis, visual disturances, AKI, bell’s palsy
Hemorrhagic stroke, HTN encephalopathy, FTT
LVH
Flash pulmonary edema

95
Q

What is surgical management of MAS?

A

patch angioplasty
reimplant of visceral vessels
TA bypass

96
Q

What size graft to use for bypass at different ages?

A

8-12mm children
12-16 early ADOLESCENTS
14-20 late adolescents and adults

97
Q

When does axial growth stop?

A

age 9-10

98
Q

How and when do you repair renal artery in children?

A

after age 3
internal iliac
(SV has aneurysmal degen)

99
Q

What is the definition of HTN in children?

A

SBP or DBP >/= 95th percentile for sex age and hgt on 3 separate occasions

100
Q

In embryology, what gives rise to the abdo aorta?

A

primitive dorsal artery

101
Q

In embryology, what gives rise to the celiac?

A

10th segmental branch

102
Q

In embryology, what gives rise to the SMA?

A

11th segmental branch

103
Q

In embryology, what gives rise to the IMA?

A

21st segmental branch

104
Q

What are the branches of the celiac?

A

left gastric
splenic
common hepatic

105
Q

What is the most frequent anatomic variation of the celiac?

A

hepatic arises from SMA or directly from aorta

106
Q

What are the branches of the SMA?

A

PDA
middle colic
right colic
ilieocolic
third order branches

107
Q

What are the branches of the IMA?

A 
sigmoidal branches 
left colic (becomes marginal artery)
108
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

109
Q

What are SMA and IMA connections?

A 
marginal artery 
meandering artery (l colic to middle colic)
110
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

111
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

112
Q

What is NOMI?

A

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

113
Q

What causes NOMI?

A

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

114
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.

115
Q

What are RF for NOMI?

A

low flow states
hypovolemia
systemic vasoconstrictirs
AI
CPB
reperfusion injury

116
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

117
Q

What are celiac-sma collaterals?

A

GDA-PDA

118
Q

What are IMA-internal collaterals?

A

hemorrhoidals to internal iliac

119
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

120
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

121
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

122
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

123
Q

What are other diagnostic test?

A

CTA/MRA
gastric tonometry

124
Q

What are positive result of gastric tonometry for CMI?

A

Reduced CO2 washout from ischemic tissue cause PCO2 to rise

125
Q

What are positive result of gastric tonometry for CMI?

A

Reduced CO2 washout from ischemic tissue cause PCO2 to rise

126
Q

What are indication for revasc for CMI?

A

symptoms
some suggest 3 VD
during aortic reconstruction

127
Q

What is advantages of endovascular?

A

likley shorter hospital stays, reduced M&M
probably less long-term patency

128
Q

What are open bypass strategies?

A

supracelia (tunnel retropancreatic, ant to L renal
retrograde from infrarenal aorta or CIA (right lays better)

129
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

130
Q

What are open bypass strategies?

A

supracelia (tunnel retropancreatic, ant to L renal
retrograde from infrarenal aorta or CIA (right lays better)

131
Q

What is median arcuate ligament syndrome?

A

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

132
Q

What is treatment for MALS?

A

division of crura with endo possibly

133
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

134
Q

What are features of AMI on X-ray?

A

Thumbprinting in advanced cases of ischemia (pneumatosis)

135
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

136
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

137
Q

What are causes of mesenteric vein thrombosis?

A

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

138
Q

What does bowel look like on inspection?

A

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

139
Q

What does bowel look like on inspection?

A

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

140
Q

What are treatment options?

A

if no peritonitis then AC with heparin
if peritonitis or bleeding, the ex lap, bowel resection

141
Q

What is in hospital mortality for MVT?

A

20%

142
Q

What are other therapeutic options for MVT?

A

TIPS
perc transhepatic tpa
thrombolysis via SMA

143
Q

What are some common cause of splanchnic aneurysms?

A

athero
FMD
CTD
inflammatory conditions
iatrogenic

144
Q

What are the most common aneurysms?

A

splenic
hepatic
SMA
celiac
Gastric

145
Q

Which have the highest rupture rate?

A

GAA 90%
HAA 20-40%
CAA 10%
SPA
high in pregnancy

146
Q

Which have the highest mortality with rupture?

A

CAA SPAA 75% in pregnancy
fetal 85%
rest >10%

147
Q

What disease has high incidence of SA?

A

polyarteritis nodosa

148
Q

What is the double rupture?

A

1st into lesser sac
2nd intraperitoneal

149
Q

What are X-ray findings of splenic artery aneurysm?

A

70% curvilinear signet ring of calcification

150
Q

What are indication to operate on splenic AA?

A

Symptomatic
Rupture
Enlarging (10% of patients)
>2cm (not absolute)
Pregnant or childbearing age
Portal HTN or liver transplant list
False aneurysm regardless of size (Cleveland Clinic)

151
Q

At what level can you ligate splenic?

A

prod-mid
collaterals from short gastric

152
Q

Why is HAA incidence increasing?

A

conservative management of blunt liver trauma and biliary procedures

153
Q

What is HAA triad?

A

abdo pain
hematobilia
obstructive jaundince

154
Q

When can you ligate a HAA?

A

if there is a patent GDA

155
Q

Where are SMAA usually located?

A

first 5 cm

156
Q

What are indications for intervention on SMAA?

A

no size per se
false aneurysm

Vascular Surgery (37 decks)

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