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

Chap 144-148 Renal Artery Stenosis/Aneurysm Flashcards

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
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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25
Q

What is middle aortic syndrome?

A

coarctation of the abdominal aorta

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26
Q

What causes middle aortic syndrome?

A

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

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27
Q

What disease associated with MAS?

A 
NF-1
williams syndrom
maternal rubella
takayasu
umbilical artery catheterization
28
Q

What stenosis are associated with MAS?

A

splanchnic 90%
RA 60%

usually ostial

29
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,
30
Q

What is the definition of HTN in children?

A

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

31
Q

What is management of MAS?

A

anti htn
patch angioplasty
reimplant viscerals
thoracoabdominal bypass

32
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

33
Q

whats the repp rate at 5-10years?

A

10%

axial growth not significant after10 yo

34
Q

What is the usual appearance/location of RA aneurysms?

A

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

35
Q

What are causes of RAA?

A 
FMD
EDS
dissections
iatrogenic
trauma
post-stenotic dilation
polyarteritis nodosa (intrarenal)
36
Q

what is presentation of RAA?

A

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

37
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
38
Q

What is mortality and patency of open repair?

A

1.7%

96% 4 year patency

39
Q

What are components of cold perfusion preservation solution?

A

KCL, NA, phosphate, Bicarb, chloride

40
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

41
Q

What is the presentation of renal AVM?

A 
hematuria (70%)
HTN
RI
high output CHF,
rupture
vague abdo/flank pain
42
Q

Which more common r or l?

A

right

43
Q

what are causes of renal AVM?

A 
congenital
acquired (biopsy 1-10% incidence, trauma, iaotro)
FMD
aneurysm/malignancy erosion
nephrectomy
44
Q

What is appearance of renal AVM on CT?

A

filling defect in kidney with dilated vessels

45
Q

When to tx? and what tx?

A

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

46
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

47
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

48
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
49
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.

50
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

51
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
52
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

53
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)

54
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

55
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

56
Q

What are abnormal values for renal vein renin assay?

A

renal vein to systemic ration

>1.5 is positive

57
Q

What is the difference in stenting vs surgery for RAS

A

MA

BP control equivalent

58
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

59
Q

What are open techniques for RAS?

A

aorto renal bypass
thromboendarterrectomy
renal artery reimplantation

hepatorenal bypass
splenorenal bypass
ex vivo reconstruction

60
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

61
Q

What are components of cold perfusion preservation solution?

A 
K
sodium
phosphate
chloride
bicarb
62
Q

What is a cortical rim sign?

A

on CTA the cortical rim is capsular perfusion from collaterals

63
Q

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

A 
KMP
Sos Omni
C1, C2
shepherd hook
simmons
JB1
64
Q

What are endovascular treatments for RA embolism?

A

CDT
aspiration
covered stent

65
Q

Which RA embolism to offer intervention?

A

acute and potentially salvageable renal function esp. bilateral embolism

66
Q

What is the mortality of surgical management for RA embolism?

A

25%

67
Q

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

A

Will need angioplasty and stenting

need bypass or endart

Vascular Surgery (53 decks)

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