vascular disorders Flashcards

(79 cards)

1
Q

atherosclerotic lesions in the extremities

Prevalence 30% in patients who are:
o >70 years old without risk factor
o 50 years old with risk factors (DM or tobacco use)

Three classic segments in lower extremities:
o Aortoiliac segment
o Femoral-popliteal segment
o Infrapopliteal or tibial segment

A

peripheral artery disease

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2
Q
  • White men aged 50-60
    years who smoke cigarettes
  • Disease progression may
    lead to complete occlusion
    of one or both common iliac
    arteries (Can precipitate
    occlusion of the entire
    abdominal aorta to the level
    of renal arteries)
A

aorta and iliac arteries

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3
Q

Symptoms:
o Pain into thigh/buttocks
o ED (bilateral common iliac disease)
o Weakness in legs when walking
o Extreme limb fatigue

Signs:
o Pain relieved with rest and reproducible when patient walks again
o Femoral pulses and distal pulses are absent or very weak
o Bruits- aorta, iliac, and femoral

A

occlusive disease: aorta and iliac arteries

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4
Q

how to diagnose occlusive disease: aorta and iliac arteries

A

Doppler & Vascular Findings
o Ankle-brachial index (ABI)

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5
Q

Segmental waveforms or pulse volume recordings
 Obtained by strain gauge technology through
blood pressure cuffs
 Demonstrate blunting of arterial inflow throughout the lower extremity

 Both dorsalis pedis and posterior tibial arteries are measured (higher of two used

A

Ankle-brachial index (ABI)

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6
Q

what is not normal for Ankle-brachial index (ABI)

A

<0.9 (normal is 0.9-1.2)

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7
Q

occlusive disease: aorta and iliac arteries treatment

A

Cornerstones of treatment –> cardiovascular risk reduction & exercise program

 Risk factor reduction
o Smoking cessation – consider nicotine replacement therapy or cessation medications
o Antiplatelet therapy
 Aspirin 81 mg
 Clopidogrel 75 mg
o Low-dose rivaroxaban 2.5 mg BID with aspirin 81 mg daily
 Reduce both major CV and limb-related adverse events in symptomatic patients
o Lipid & blood pressure control
 High-dose statin (atorvastatin 80 mg daily)
o Cilostazol 100 mg BID
 May improve walking distance in 2/3 of patients (may take 2-4 weeks to be effective and 12 weeks
until full effect)
o Weight loss

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8
Q

occlusive disease: aorta and iliac arteries treatment surgical intervention

A

prosthetic aorta femoral bypass graft

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9
Q

When to admit for occlusive disease: aorta and iliac arteries

A

o Evidence of chronic limb-
threatening ischemia
 Lower extremity rest pain and
tissue loss
o Patients with acute limb ischemia
 Will need IV anticoagulation
and surgical consult

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10
Q
  • Superficial femoral artery-
    MC occluded by
    atherosclerosis
  • 1 decade after development
    of aortoiliac disease
  • Men=Women
  • MC in Black and
    Latino/Latina patients
A

femoral and popliteal arteries

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11
Q

Intermittent claudication confined to calf
o There are some good collateral vessels that can be maintained but when they become
occluded-shorter distances may trigger symptoms
 Present with dependent rubor of foot (if you raise the foot, the redness will go away)

  • Chronic low blood flow- atrophic changes in lower leg
    o Loss of hair
    o Thinning of skin and subcutaneous tissues
    o Disuse atrophy of muscles
  • With segmental disease of superficial artery
    o Common femoral pulsation normal
    o Popliteal and pedal pulses reduced
A

occlusive disease: femoral and popliteal arteries signs and symptoms

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12
Q

how to diagnose occlusive disease: femoral and popliteal arteries

A

 Doppler & Vascular Findings
o ABI <0.9 diagnostic
 Levels <0.4 suggest chronic limb-threatening ischemia

 Imaging
o Duplex ultrasound, CTA and MRA
o Only performed if revascularization is planned
 After revascularization- patients monitored with annual ultrasoun

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13
Q

occlusive disease: femoral and popliteal arteries treatment

A

 Medical & Exercise Therapy
o Risk factor reduction
 Antiplatelet
 High-dose statin
 Exercise treatment
 Dual treatment with rivaroxaban 2.5 mg BID and aspirin 81 mg daily
 Reduce limb-related events, major amputation, and CV events

o Symptom treatment
 Cilostazol 100 mg BID- improves intermittent claudication symptom

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14
Q

occlusive disease: femoral and popliteal arteries surgical intervention

A

Indications: progressive claudication, incapacitating, interferes significantly with essential
daily activities or employment
o Mandatory if ischemic rest pain or ischemic ulcers threaten foot

o Bypass Surgery
 Femoral-popliteal bypass (most effective and durable)
 Uses autologous saphenous vein

o Endovascular Techniques
 Angioplasty and stenting
 Most effective in patients undergoing aggressive risk factor modification in whom lesions measure
<10 cm long

o Thromboendarterectomy
 Removal of plaque- limited to lesions of common femoral and the profunda femoris arter

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15
Q

Complications of occlusive disease: femoral and popliteal arteries

A

o Wound infection
o Seroma
o MI rates after open surgery are 5-10%, with 1-4% mortality
o Complication rates of endovascular surgery are 1-5% (makes these more attractive despite their
lower durability)

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16
Q

occlusive disease: femoral and popliteal arteries when to refer

A

o Progressive symptoms
o Short-distance claudication
o Rest pain
o Ulceration

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17
Q

occlusive disease: femoral and popliteal arteries when to admit

A

o Chronic limb threatening ischemia (rest pain, tissue loss)
o Foot infection

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18
Q
  • Diabetic patients
  • Extensive calcification
  • Claudication may NOT be
    present
A

tibial and pedal arteries

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19
Q

o Ischemic ulcer or foot gangrene first manifestation
 WONT present with claudication
o Ischemic rest pain- confined to dorsum of foot (relieved with dependency)
 Pain does not occur with standing, sitting, or dangling leg over edge of bed
 Severe and burning in character
 May awaken the patient from sleep
o Femoral and popliteal pulses may/may not be present
o Absent pedal pulses
o Dependent rubor with pallor on elevation
o Skin of foot- cool, atrophic, hairless

A

occlusive disease: Tibial and pedal arteries signs and symptoms

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20
Q

how to diagnose occlusive disease: Tibial and pedal arteries

A

digital subtraction angiography is gold standard

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21
Q

occlusive disease: Tibial and pedal arteries treatment

A

 Treatment
o Prevent ulcers
o Revascularization to avoid major amputation if
ulceration appears and is not healing within 2-3
weeks
 Bypass and Endovascular Techniques
o Bypass- saphenous vein
 Can treat rest pain and heal ischemic foot ulcers
 Amputation

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22
Q

When to admit occlusive disease: Tibial and pedal arteries

A

o ANY patient with DM and foot ulcer and infection
(emergent incision and drainage)
o Broad-spectrum antibiotics empirically
 Vanco + ertapenem or pip/taz

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23
Q

 Can be due to embolus or to thrombosis of a diseased atherosclerotic segment
o Emboli- often cardiac in origin
 >50% of emboli from heart go to LE
 20% to cerebrovascular circulation
 Remainder go to upper extremities and mesenteric and renal circulation
 Afib MC cause of cardiac thrombus formation
 Patient with primary thrombosis will have history of claudication and an abrupt worsening of symptoms

A

acute arterial occlusion of a limb

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24
Q

o Sudden onset of extremity pain
o Loss or reduction in pulses
o Neurologic dysfunction—numbness, paralysis
o Pallor, coolness of extremity, mottling
o The 5 “P’s”– pain, pulselessness, pallor, paresthesia, paralysis
o Poikilothermia is the 6th

A

signs and symptoms of acute arterial occlusion of a limb

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25
doppler and lab findings of acute arterial occlusion of a limb
 Doppler & Laboratory Findings o Little to no flow on doppler of distal vessels o Blood work- myoglobinemia and metabolic acidosis  Imaging o Done in operating room  Obtaining angiography, MRA, or CTA may delay revascularizatio
26
acute arterial occlusion of a limb treatment
 IMMEDIATE revascularization  Heparin (as soon as diagnosis is made) o ASAP-initial IV bolus of unfractionated heparin (80 U/kg)  Followed by continuous heparin infusion to maintain aPTT in therapeutic range (60-85 sec)- about 12- 18 units/kg/hr o Prevents clot propagation o May relieve associated vessel spasm o Revascularization will still be required  Endovascular Techniques o Pharmacomechanical thrombectomy catheters o Catheter-directed chemical thrombolysis with TPA o Immediate revascularization  Surgical intervention under general anesthesia
27
acute arterial occlusion of a limb prognosis
 Risks for acute arterial embolic occlusion  10-25% risk of amputation  25% or higher in-hospital mortality rate  Prognosis for acute thrombotic occlusion of an atherosclerotic segment is generally better because the collateral flow can maintain extremity viability
28
 Segmental, inflammatory, and thrombotic process of distal-most arteries and occasionally veins of the extremities  Pathologic examination- arteritis in affected vessels  Cause- unknown o Rarely seen in patients who do not smoke cigarettes  Arteries MC affected- plantar and digital vessels of foot and lower leg o In advanced stages- fingers and hands may become involved
thromboangiitis obliterans (burger disease)
29
o Similar to peripheral vascular disease o Patient <40 years o Superficial thrombophlebitis (will discuss later in this lecture) o Intermittent claudication is NOT common- rest pain is frequent
signs and symptoms of burger disease
30
burger disease diagnosis
MRA or invasive angiography- obliteration of distal arterial tree
31
burger disease treatment
Cessation of cigarette smoking is mainstay of therapy
32
 Can be atherosclerotic or inflammatory  Aorta of a healthy young man measures about 2 cm  Aneurysm is considered present with aortic diameter >3 cm o Rarely rupture until diameter exceeds 5 cm  Found in 2% of men >55 years of age  Male: Female is 4:1  90% originate below the renal arteries o Usually involve aortic bifurcation and common iliac arteries
abdominal aortic aneurysm (AAA)
33
o Asymptomatic  80% of 5-cm infrarenal aneurysms are palpable on routine PE  Most found on US or CT imaging incidentally or as screening  May have thick layer of thrombus lining the aneurysmal sac- embolization to LE rare  Symptomatic o Pain  Mild-severe midabdominal pain radiating to lower back  Constant or intermittent and exacerbated by gentle pressure on aneurysmal sac o Rupture  Severe pain and hypotension (blood escapes into retroperitoneal space)
signs and symptoms of AAA
34
AAA lab findings
o Acute rupture- hematocrit may be normal still o May have CAD, carotid disease, kidney disease, emphysema  Preoperative testing may indicate presence of these comorbid condition
35
AAA diagnosis
 Abdominal ultrasound- diagnostic study of choice for initial screening  CT scans provide more reliable assessment of diameter o Done when diameter nears threshold for treatment (5.5 cm) o Contrast-enhanced show arteries above and below – helps plan repair o Often demonstrate mural thrombus within the aneurysm- anticoagulation NOT indicated
36
AAA monitoring if they have an aneurysm
 Once identified- routine ultrasound should be done- frequency depends on size o 3-3.9 cm --> every 3 years o 4-4.9 cm --> every 12 months o 5 cm or larger --> every 6 months  When reaches 5 cm- CTA with contrast should be done to define arterial anatomy and more accurately assess aneurysm size
37
who do we screen for AAA
o Ultrasound o Men 65-75 years old  With exposure to 100 or more lifetime cigarettes o If aorta 2-2.9 cm- repeat 10 years
38
AAA treatment o Indicated for AAA 5.5 cm or larger in men or 5 cm in women o Aneurysmal growth (>0.5 cm in 6 months) o Symptoms- pain or tenderness (urgent repair regardless of diameter)
Elective Repair
39
AAA when to refer/admit
 Refer o 4.5 cm or larger aortic aneurysm o Pain confined by gentle palpation of aneurysm (regardless of size)  Admit o Tender aneurysm to palpation or signs of aortic rupture o Evidence of infection after repair
40
most common cause of thoracic aorta aneurysms
atherosclerosis
41
 Symptoms/Signs o Most are asymptomatic o Substernal back/neck pain o Pressure on trachea, esophagus, superior vena cava  Dyspnea, stridor, brassy cough, dysphagia, edema in neck and arms, distended neck veins o Stretching of left recurrent laryngeal nerve  Hoarseness o Rupture- lethal- bleeding rarely contained (allows no time for emergent repair)
thoracic aortic aneurysms
42
thoracic aortic aneurysms diagnostics
CT scan with contrast- modality of choice for anatomy and size
43
thoracic aortic aneurysms treatment
 Proximal aortic arch/ascending aorta o Repair when 5.5 cm o Open surgery required due to requirement of interruption of arch blood flow  Descending aorta o Repair considered when 5.5 cm or larger o 5-year survival is 54% in untreated patients o Endovascular grafting
44
thoracic aortic aneurysms complications
o Endovascular repair- discrete saccular aneurysms of descending thoracic aorta o Morbidity and mortality higher than infra-renal AAA repair o Paraplegia o Stroke risk increased when involvement of the aortic arch
45
thoracic aortic aneurysms when to refer
o Ascending >4.5 cm o Descending at 5 cm
46
 Popliteal artery aneurysms 70%  May embolize repetitively over time and occlude distal arteries  Primary femoral artery aneurysms are less common  Pseudoaneurysms of femoral artery following arterial punctures for arteriography and cardiac may occur
peripheral artery aneurysms
47
 Pulsatile mass when in groin (popliteal aneurysms go undetected)  Compressive symptoms (rare)  First symptom may be due to ischemia of acute arterial occlusion  Prominent or easily felt pulse in popliteal artery is suggestive- get ultrasound  Popliteal aneurysms are bilateral in 60% of cases  About 50% of patients with popliteal aneurysms have AAA
peripheral artery aneurysms
48
peripheral artery aneurysms diagnostics
 Duplex color ultrasound  MRA or CTA  Arteriography NOT recommended  Abdominal ultrasound if popliteal aneurysm found to evaluate for AAA**
49
peripheral artery aneurysms treatment
 Immediate or urgent surgery when acute embolization or thrombosis has caused acute ischemia  Open surgical bypass  Surgery indicated when:  Associated with peripheral embolization  >2 cm  Mural thrombus present  Acute pseudoaneurysms of femoral artery due to arterial punctures  Ultrasound-guided compression or thrombin injection  Open surgery with prosthetic interposition grafting is preferred for primary aneurysms of femoral artery
50
 Spontaneous intimal tear- blood dissects into media of aorta  Results from repetitive torque  Hypertension  Classified by entry point and distal extent  Type A dissection  Type B dissection  Increased risk in:  Pregnancy  Bicuspid aortic valve  Bovine arch  Coarctation
aortic dissection
51
what is different about the bovine aortic arch anomaly
LCCA comes off brachiocephalic
52
aortic dissection treatment
 TRUE EMERGENCY- requires IMMEDIATE control of blood pressure to limit extent of dissection  Type A has worse prognosis  Death in hours- rupture of dissection extends into pericardial sac or coronary arteries – results in MI  Rupture into pleural cavity is also possible  Intimal/medial flap created by dissection may occlude major aortic branches  Ischemia of brain, intestines, kidney, or extremities
53
 Severe persistent chest pain (sudden onset)- radiates down back or into anterior chest- possibly into neck  Hypertension  Syncope  Hemiplegia  Paralysis of lower extremities  Mesenteric ischemia or kidney injury  Peripheral pulses diminished or unequal  Diastolic murmur  Dissection in ascending aorta close to aortic valve  Valvular regurgitation  Heart Failure  Cardiac tamponade
aortic dissection
54
aortic dissection diagnostics
Multiplanar CT with contrast- (chest, abdomen, and pelvis)
55
aortic dissection treatment
 Aggressive blood pressure lowering (even before diagnostic studies)  Systolic: 100-120 mm Hg  Heart rate: 60-70 bpm  BB are 1st line- reduce LV ejection force  Labetalol (IV)
56
type A aortic dissection surgical treatment
 Urgent  Transfer to appropriate facility if skilled CV team not available
57
Type B dissection with malperfusion aortic dissection treatment
 Urgent if there is aortic branch compromise (resulting in malperfusion of renal, visceral, or extremity vessels)
58
Type B dissection without malperfusion aortic dissection treatment
 Blood pressure control is primary treatment
59
 Dilated, tortuous superficial veins in the legs  Periods of high venous pressure  Prolonged standing or heavy lifting  Following pregnancy  Develop in >20% of adults  Distention of vein prevents valve leaflets from coming together- creates incompetence and reflux of blood towards the foot  Congenital or acquired  Consider AV fistulas or venous malformations in young patients presenting with varicosities
varicose veins
60
 Signs/Symptoms  Severity is NOT correlated with number and size of varicosities  Dull, aching heaviness, feeling of fatigue in the legs  Worse with periods of standing  Itching from venous eczema above ankle or directly overlying large varicosities  Dilated, tortuous veins of thigh and calf  Chronic venous insufficiency  Ankle edema, brownish skin hyperpigmentation, chronic skin induration or fibrosis
varicose veins
61
varicose veins diagnostics
 Duplex ultrasound  Most cases – reflux arises from the greater saphenous vein
62
varicose veins treatment
Nonsurgical  Compression stockings (20-30 mm Hg pressure) Sclerotherapy  Direct injection of sclerosing agent – permanent fibrosis and obliteration of target veins  Complications- phlebitis, tissue necrosis, infection Surgical  Vein stripping (removal)  Endovenous treatments  Thermal devices (laser or radiofrequency catheter)  Complication of thermal tx- DVT- may require prolonged anticoagulation  Cyanoacrylate glue injection  Foam sclerosant injection
63
 Inflammation of a vein just below surface of the skin- resulting from a blood clot  MC causes:  Short-term IV in superficial veins  Long-term PICC lines  IV sites should be observed daily and removed if local reaction develops  Serious thrombotic or septic complications can occur if this is not done  MC pathogen- S. aureus  Can also occur spontaneously  Pregnancy, postpartum, varicose veins, trauma  Can be a manifestation of systemic hypercoagulability secondary to abdominal cancer (pancreatic cancer)- may be earliest sign of these conditions
superficial venous thrombophlebitis
64
 Signs & Symptoms  Dull pain  Induration, redness, tenderness of vein  Firm cord (usually once inflammation has resolved)  Edema of extremity is uncommon  Proximal extension of induration and pain with chills and high fever  Septic phlebitis- urgent treatment required
superficial venous thrombophlebitis
65
superficial venous thrombophlebitis diagnostics
ultrasound
65
superficial venous thrombophlebitis treatment
 Focal/spontaneous (usual course 6 weeks)  Local heat and NSAIDs  Prophylaxis with fondaparinux or rivaroxaban  5 cm or longer of saphenous vein  Full anticoagulation  Reserved for disease that is rapidly progressing or concern for extension into deep system  Indicated for active malignancy, history of venous thromboembolism, and known thrombophilia  If induration is extensive, progressing towards saphenofemoral junction (leg), or cephalo-axillary junction (arm) despite anticoagulation  Ligation and division of vein at junction of deep and superficial veins is indicated
66
superficial venous thrombophlebitis treatment if septic
 Septic- considered intravascular abscess  Urgent treatment with heparin or fondaparinux  Remove offending catheter  Antibiotics  Vancomycin, 15 mg/kg IV every 12 hours + ceftriaxone, 1 g IV every 24 hours  If cultures positive- continue for 7-10 days or 4-6 weeks if complicating endocarditis cannot be excluded  Surgical excision may be necessary to control infection
66
 Severe manifestation of venous HTN  MC etiology  Prior DVT  Although, 25% of patients do not have a known history of DVT  Other etiologies  Leg trauma or surgery  Obesity (complicating factor)  Progressive superficial venous reflux  Congenital or neoplastic obstruction of pelvic veins  Congenital or acquired arteriovenous fistula
chronic venous insufficiency
67
 Valve leaflets can be:  Thickened and scarred (post-thrombotic syndrome)  Nonfunctioning in a dilated vein  Signs & Symptoms  Progressive pitting edema is primary presenting symptom  Secondary skin changes  Itching  Dull discomfort made worse by periods of standing  Pain if ulceration is present  Skin at ankle taunt from swelling, shiny, brownish pigmentation  Varicosities  Cellulitis
chronic venous insufficiency
68
chronic venous insufficency diagnostics
duplex ultrasound
69
chronic venous insufficiency treatment
 Prevention  Early and aggressive anticoagulation of acute DVT  Compression stockings if chronic edema develops after DVT has resolved  Treatment- General measures  Compression stockings (20-30 mm Hg or higher)  Avoid prolonged standing or sitting  Intermittent elevations of involved leg  Sleep with legs above level of heart  Pneumatic compression of the leg  Cellulitis treatment (cephalexin/clindamycin)  Ulcer treatment  Vein treatment (reflux or obstruction)
70
Blood clot obstructing blood flow in deep venous system  MC in legs  Can be provoked  Recent surgery or trauma  Hospitalization with prolonged bed rest  Use of oral contraceptives  Can be unprovoked  Idiopathic  Inherited or acquired hypercoagulable states (cancer and pregnancy)
deep vein thrombosis
71
DVT risk factors
 Risk Factors  Virchow's Triad  Wall damage  Venous stasis  Hypercoagulability
71
 Isolated to deep veins below the knee  Lower rates of recurrence, PE and development of post-thrombotic syndrome
distal DVT
72
 Extends into popliteal vein or more proximally  Majority of DVTs
proximal DVT
73
 Signs/Symptoms  May be asymptomatic  Pain, swelling, warmth, redness of lower extremity  Well’s Criteria
DVT signs
73
 Involves partial or complete thrombosis of iliac or common femoral veins  May/may not include other lower extremity veins or inferior vena cava  Associated with more severe symptoms, risk of recurrent VTE, and increased severity of post-thrombotic syndrome
 Iliofemoral DVT (subtype of proximal
74
DVT diagnostics
 D-dimer  Compression ultrasound
75
DVT treatment
 Goal is to prevent recurrence or development of complications (PE and post- thrombotic syndrome) while limiting bleeding risk  Initial management of DVT:  Isolated distal DVT: benefits of anticoagulation therapy are unclear (low risk of progressive or recurrent DVT)  If severe symptoms or risk for extension- consider anticoagulation x 3 months  No severe symptoms- serial imaging of deep veins for 2 weeks  Proximal DVT:  Anticoagulant for 3 or more months  Dabigatran, rivaroxaban, apixaban, edoxaban  Iliofemoral DVT:  Anticoagulant for 3 or more months  Consider catheter-directed pharmacomechanical thrombectomy if symptoms do not resolve