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Vascular Surgery > Chap 144-148 Renal Artery Stenosis/Aneurysm > Flashcards

Chap 144-148 Renal Artery Stenosis/Aneurysm Flashcards

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0
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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1
Q

How many patients have bilateral RAS? Have complete occlusion?

A

12%

12%

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2
Q

What factors are associated with progression?

A

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

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3
Q

What is the pathogenesis of RAS?

A

athero 80%
FMD 15%
dissection 1%

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4
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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5
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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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
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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14
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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15
Q

Who benefits most from interventions?

A

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

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16
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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17
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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18
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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19
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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20
Q

What are consequences of thromboses renal vein?

A

acute renal ischemia from

congestion and edema

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21
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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22
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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23
Q

What is treatment for RA embolism or thrombosis?

A

AC alone unless bilat or solitary kidney

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24
What are the results of AC for RA thrombosis? for OR?
1 month mort 10% 60% normal renal function at long-ten follow-up 8% required dialysis 25% mortality with open
25
What is middle aortic syndrome?
coarctation of the abdominal aorta
26
What causes middle aortic syndrome?
over fusion of the two dorsal aortas during 4th week of gestation
27
What disease associated with MAS?
``` NF-1 williams syndrom maternal rubella takayasu umbilical artery catheterization ```
28
What stenosis are associated with MAS?
splanchnic 90% RA 60% usually ostial
29
What are clinical features of MAS?
``` HTN (HA, seizure, AKI, bell's palsy,) lower extremity fatigue (uncommon) FTT intestinal angina LVH, flash PE, ```
30
What is the definition of HTN in children?
SBP or DBP >95th percentile for sex age and hgt
31
What is management of MAS?
anti htn patch angioplasty reimplant viscerals thoracoabdominal bypass
32
What sized graft to use for TA bypass for children, adolescents and adults?
8-12mm children 12-16 early adolescents 14-20 late adol, adults
33
whats the repp rate at 5-10years?
10% | axial growth not significant after10 yo
34
What is the usual appearance/location of RA aneurysms?
true 90% extraparenchymal 75% saccular usually at main renal artery bifurcation
35
What are causes of RAA?
``` FMD EDS dissections iatrogenic trauma post-stenotic dilation polyarteritis nodosa (intrarenal) ```
36
what is presentation of RAA?
asympto 1/3 with symptoms HTN, flank pain, hematuria, rupture RI with distal emboli or compression
37
What are indications for intervention?
``` >2-3cm rupture (10% mortality) consider if pregnant HTN---DBP >90 despite 3 anti-HTN Dissection if viability threatened ```
38
What is mortality and patency of open repair?
1.7% | 96% 4 year patency
39
What are components of cold perfusion preservation solution?
KCL, NA, phosphate, Bicarb, chloride
40
what is polyarteritis nodosa?
medium sized arterial vessel vasculopathy that cause small aneurysms that are strung like beads (rosary sign) tx cyclophosphamide and steroids
41
What is the presentation of renal AVM?
``` hematuria (70%) HTN RI high output CHF, rupture vague abdo/flank pain ```
42
Which more common r or l?
right
43
what are causes of renal AVM?
``` congenital acquired (biopsy 1-10% incidence, trauma, iaotro) FMD aneurysm/malignancy erosion nephrectomy ```
44
What is appearance of renal AVM on CT?
filling defect in kidney with dilated vessels
45
When to tx? and what tx?
after bx most close spon within one year most don't require tx consider if HTN
46
What is difference in pathophys in bilateral and unilateral RAS and RV-HTN?
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
47
what are clinical characteristics of RV-HTN?
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
48
list causes of RV-HTN. which are 3 most common?
RAS FMD dissection Takayasu (sub-continent and far east ``` hypoplastic/MAS in children Emboli Trauma Ligation during surgery Extrinsic compression ```
49
How does captorpil renogram work? what abnormal/normal rest?
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.
50
What are signs/symptoms of RV-HTN?
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
51
What are RF for contrast-induced nephrotoxicity?
``` Age CKD Diabetes mellitus Hypertension Metabolic syndrome Anemia Multiple myeloma Hypoalbuminemia Renal transplant Hypovolemia and decreased effective circulating volumes Urgent Volume of contrast ```
52
Define resistive index? how do yo calculate? What are normal values?
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
53
What are the mechanisms by which AII causes HTN?
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)
54
What are the effects on the unaffected kidney in RAS?
exposure to sustained HTN and circulating ATII and aldosterone efferent and afferent arteriolar vasoc sustained decrease in glomerular filtration afferent arteriolar hypertrophy and arteriosclerosis
55
How does renal vein renin assays work?
stop antiHTN give lasix night before catheter in each renal vein and one in IVC reference sample then samples q5mins x2
56
What are abnormal values for renal vein renin assay?
renal vein to systemic ration | >1.5 is positive
57
What is the difference in stenting vs surgery for RAS
MA | BP control equivalent
58
Who to treat for RAS?
uni-if severe HTN and low risk bilat but one kidney sever-treat like uni disease bilat severe-htn severe and renal dysfunction
59
What are open techniques for RAS?
aorto renal bypass thromboendarterrectomy renal artery reimplantation hepatorenal bypass splenorenal bypass ex vivo reconstruction
60
What are the results of the CORAL trial?
stenting showed no benefit over PMT in reducing death or MACE in RAS STAR and ASTRAL trial demonstrated the same
61
What are components of cold perfusion preservation solution?
``` K sodium phosphate chloride bicarb ```
62
What is a cortical rim sign?
on CTA the cortical rim is capsular perfusion from collaterals
63
What are catheters that can be used to select the renals?
``` KMP Sos Omni C1, C2 shepherd hook simmons JB1 ```
64
What are endovascular treatments for RA embolism?
CDT aspiration covered stent
65
Which RA embolism to offer intervention?
acute and potentially salvageable renal function esp. bilateral embolism
66
What is the mortality of surgical management for RA embolism?
25%
67
How is the management of RA thrombosis different to Renal artery embolism?
Will need angioplasty and stenting | need bypass or endart

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