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30 Cards in this Set
- Front
- Back
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Unilateral renovascular disease
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The kidney that is affected by the stenosis experiences reduced renal perfusion which activates its renin angiotensin system.
This leads to an increased production in angiotensin II and aldosterone leading to an angiotensin II dependent hypertension. The contralateral kidney experiences increased perfusion which leads to suppression of its own renin angiotensin system and increased sodium excretion (a so called pressure natriuresis) which results from the hyperfiltration resulting from the higher blood pressure being driven by the opposite kidney. When blockade of the renin angiotensin system occurs through the use of ACE inhibitors or angiotensin receptor blockers there is a reduced arterial pressure and the glomerular filtration rate in the kidney affected by the stenosis may fall. The use of these agents also will lead to enhanced lateralization on various functional diagnostic tests and we will touch on this more later as well. It is important to note that lateralization on functional tests occurs in unilateral disease but not bilateral disease. |
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Bilateral renovascular disease
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When both kidneys are affected each kidney sees reduced renal perfusion.
It is important to note that stenosis of a solitary kidney is effectively the same as bilateral stenosis as the entire renal mass is affected. With the entire renal mass seeing hypoperfusion the renin angiotensin system is activated, but in this situation there is no remaining normal kidney that can hyperfiltrate and excrete the excess sodium. This leads to impaired sodium and water excretion which leads to a significant volume expansion which separates bilateral renal artery stenosis from unilateral stenosis. This volume expansion coupled with the angiotensin II mediated effects leads to severe hypertension. With blockage of the renin angiotensin system in these patients you will see reduced arterial pressure only after the patient has some volume depletion usually through the effects of diuretics. Renin angiotensin system blockade may also lead to precipitous decreases in GFR and acute renal failure in these patients. It is important to note that functional tests in these patients will not lateralize as the entire renal mass is affected. |
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Angiotensin receptors
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AT1R
Widely distributed -kidney, vascular wall, adrenals, heart brain, lung, liver -G-protein coupled -Multiple regulators --ATII --LDL --Insulin --Estrogen --Progesterone --Interferon-γ Effects -Vasoconstriction -Pro-inflammatory -Volume expansion -Sodium retention AT2R Antagonizes effects associated with AT1R binding Primarily expressed in fetal tissues -Developmental functions Role in adult pathophysiology unclear |
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RAS clinical manifestations
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Asymptomatic
Secondary hypertension Impaired renal function Hypertensive emergency -target organ damage Acute postoperative hypertension Ventricular remodeling/diastolic dysfunction |
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Fibromuscular dysplasia
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Aortic stenosis and aneurysms
Beads on a string Best treatment is angioplasty with or without stenting |
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Natural history of RAS
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Relatively low rates of progression
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Prophylactic renal intervention
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Unassociated with clinical sequelae
Presumes -Lesion will progress -Disease progression causes loss of renal function that cannot be fully retrieved -Natural history of post-intervention renal artery superior to medical management |
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Management of RAS
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Controversial
Surgery -angioplasty and stenting superior to angioplasty alone Medical therapy -adequate for majority of patients -should be implemented prior to any consideration of procedural intervention -goals of smoking cessation, bp control, cv risk reduction -ACE inhibitors/angiotensin receptor antagonits, statins, antiplatelet |
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ACE inhibitors/angiotensin receptor antagonists and RAS
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Mainstay of therapy
Improved survival Cardiovascular event reduction Renoprotective effects -Diabetes Acute deterioration in renal function after initiation is rare |
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Statins and RAS
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Atherosclerotic renal artery stenosis
-72% reduction in risk of anatomic progression -65% reduction in risk of restenosis after endovascular treatment |
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Antiplatelet medications and RAS
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Reduced adverse cardiovascular events
Freedom from coronary stent thrombosis Reduction in procedure-related atheroembolism during renal angioplasty/stenting |
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Endovascular management of RAS and clinical response
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Renal function
-improvement is rare -post-intervention decline is serious Hypertension -cure is rare -most patients improve |
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Restenosis follwing renal angioplasty/stenting
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17-44% incidence (!)
Reported predictors: -Renal artery diameter -Stent diameter -Weight/body mass index -Smoking -Statin Use -Preoperative blood pressure |
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Surgical management of RAS
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Bypass
Thromboendarterectomy High perioperative mortality and morbidity (3-8%, 7-30%) |
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Surgical management of RAS and clinical response
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Renal function
- 26-58% early improvement - 3-27% worsen HTN -highly variable -most patients categorized as improved |
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Mesenteric ischemia pathophysiology
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Mesenteric smooth muscle tone
-Dynamic -Autoregulated extensively --10% of cardiac output at rest --35% of cardiac output after large meal Mesenteric ischemia=inadequate blood flow to visceral tissues -Acute -Chronic --Loss of compensatory autoregulation |
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Acute arterial mesenteric ischemia: etiology
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Embolism
-Heart -Aortic aneurysm or atheroma Thrombosis -Underlying proximal atherosclerosis Other -Dissection -Mesenteric aneurysm -Vasculitis |
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Acute arterial mesenteric ischemia presentation and diagnosis
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>60 years old
Severe abdominal pain (95%) -“out of proportion to exam” -Often >24h between onset and evaluation Nausea and diarrhea (30-40%) Hematochezia (15%) Shock/acidosis (<10%) |
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Acute arterial mesenteric ischemia management
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Assessment of bowel viability
-Resection of overtly necrotic bowel -Repeat exploration --~50% of patients undergo further resection at time of 2nd look Revascularization -Embolectomy -Thrombectomy -Bypass -Angioplasty/stenting -Thrombolysis (?) |
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Acute mesenteric ischemia: non-occlusive
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Intestinal gangrene despite open arteries
-May also occur with atherosclerotic disease that is not hemodynamically significant Contributing factors -Vasopressors -Cocaine -Digitalis Difficult to define Limited evidence to guide management -Antibiotics -Catheter-directed vasodilator infusion Most important strategy is to correct underlying cause -Abdominal compartment syndrome -Congestive heart failure -Sepsis Mortality predictors -Atrial fibrillation -Congestive heart failure -Recent surgery |
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Chronic mesenteric ischemia: etiology
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Atherosclerosis
-Usually affects origin of mesenteric arteries -Symptoms usually associated with multivessel disease Risk factors -Hypertension -Smoking |
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Chronic mesenteric ischemia: clinical presentation
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40-70 years old
More often female Abdominal pain (95%) -Post-prandial -10-30 minutes after eating -Mid-abdomen Weight loss (84%) Food fear |
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Chronic mesenteric ischemia: diagnosis
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Clinical history
Physical examination Imaging Duplex ultrasound -Celiac velocity >200cm/sec -SMA velocity >275cm/sec -Reversal of hepatic or splenic flow MRA CTA Arteriography |
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Chronic mesenteric ischemia surgical treatment
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Anatomic options:
-Antegrade bypass --supraceliac aorta -Retrograde bypass --Infrarenal aorta --Iliac artery -Transaortic endarterectomy --Multi-vessel disease --Extensive aortic disease High mortality and morbidity (3-29%, 12-60%) but good 12 month patency (>90%) |
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Chronic mesenteric ischemia endovascular treatment
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Perioperative death, complication rates comparable with open repair*
Symptomatic improvement -Immediate: 85% -One year: 75% Postintervention bowel ischemia requiring resection 5% -Almost uniformly fatal |
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Mesenteric venous thrombosis clinical presentation
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Acute
Pain Nausea Vomiting Abdominal distension Fever Insidious onset Delayed presentation (5-30 days) Slow progression of symptoms Chronic Incidental CT finding Portal hypertension |
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Mesenteric venous thrombosis risk factors
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Hypercoagulable states
Oral contraceptive use Neoplasms Inflammatory bowel disease Intra-abdominal inflammation Smoking Alcohol abuse Prior MVT Portal hypertension Prior abdominal surgery |
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Mesenteric venous thrombosis diagnosis
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Lab testing
-unreliable for diagnosis Radiographic -CT imaging is test of choice |
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Mesenteric venous thrombisis treatment
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Anticoagulation
Broad spectrum antibiotics Surgical exploration -Bowel gangrene |
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Mesenteric venous thrombisis surgical management
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Findings:
-Mesenteric edema -Cyanotic bowel Resect overtly necrotic bowel Liberal use of 2nd look SMV thrombectomy? -High failure rate Thrombolysis |
