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Vascular Flashcards

1
Q

What to think of: DVT and TIA/stroke?

A

Paradoxical embolus: travels from vein to R heart, across PFO to L heart and then to carotid artery

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2
Q

What promotes atherosclerotic plaque buildup at arterial branch points?

A

Low shear stress

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3
Q

How does carotid stenosis cause symptoms typically, and what are those symptoms?

A

Atherosclerotic emboli from ICA at carotid bifurcation symbolize distally to brain
Symptoms are NOT due to reduction in blood flow, and are NOT dizziness, HA, syncope

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4
Q

What determines whether brain ischemia symptoms are TIA or permanent (stroke)?

A

Size of embolus and body’s fibrinolytic system

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5
Q

If patient has had multiple TIAs with the same symptoms each time, what is the most likely source of TIA?

A

Carotid artery. Blood flows in concentric laminar rings and particles that enter the blood stream at the same point location consistently lodge distally at the same terminal branch point

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6
Q

What happens when internal carotid artery occludes?

A

No symptoms, TIA or stroke depending on where the clot stops

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7
Q

How useful is bruit to detect carotid artery stenosis?

A

Sensitivity 60-98%. Also need carotid duplex scan!

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8
Q

What is diagnostic test of choice for workup of possible carotid stenosis?

A

Carotid duplex scan + CT angiogram/MR angiogram if surgery needed

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9
Q

What are 3 management options of carotid stenosis (symptomatic)?

A

Medical management (ASA, clopidogrel, statin)
Carotid endarterectomy
Carotid artery stenting

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10
Q

How do we treat symptomatic carotid artery stenosis of 100%, 70-99% and < 70%?

A

100% medial management: ASA, statin and/or clopidogrel

70-99% carotid endarterectomy`

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11
Q

After stroke or TIA, what is the optimal timing of CEA?

A

w/in 2 weeks

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12
Q

At what percent of ICA stenosis should CEA be considered in asymptomatic patients?

A

80-99%

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13
Q

What is management of asymptomatic carotid artery stenosis in 100%, 60-99% and < 59%?

A

100%: medical: ASA, statin and/or clopidogrel
60-99%: CEA for men, medical management for women
<59%: ASA, statin, and/or clopidogrel

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14
Q

Why is there less benefit from CEA in women?

A

Women more likely to have unfavorable outcomes, likely due to smaller caliber vessels that can develop recurrent stenosis and preoperative carotid thrombosis

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15
Q

Why is BP control important prior to CEA?

A

Poorly controlled BP can increase risk of preoperative stroke
Manipulation of carotid artery/sinus during CEA can disrupt baroreceptor function
Severe postop HTN can increase risk of cerebral hyperperfusion syndrome - due to ischemia-reperfusion injury

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16
Q

Why should carotid artery stenting be considered vs. carotid endarterectomy?

A
  • Originally for patients at high surgical risk, but found to have more risk of preoperative stroke.
  • Now: those with symptomatic ICA stenosis who have hostile neck the would make surgery more difficult
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17
Q

Should CEA be done for any asymptomatic ICA stenosis?

A

Only if patient has >80% stenosis and life expectancy of > 5 years in a surgery center with perioperative complication risk of <3%.
Otherwise, medical management.

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18
Q

What is the most common cause of death in patients with carotid stenosis?

A

MI

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19
Q

How does ICA stenosis cause neurologic symptoms?

A

Secondary to embolization of atherosclerotic debris to anterior circulation

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20
Q

What is the differential for calf pain with walking?

A 
Claudication
OA of knee
Spinal stenosis
Sciatica
Chronic venous stasis
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21
Q

What is claudication?

A

Reduction in blood flow to leg muscles, most often derived from atherosclerotic plaque

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22
Q

What are the 3 important parts of claudication needed in history?

A

1 Pain in leg with walking
2 Relieved w/ few minutes of rest
3 Reproducible at walking the same distance each time

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23
Q

What is the spectrum of severity in PAD called?

A

Rutherford classification of chronic limb ischemia

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24
Q

What is ischemic rest pain?

A

Advanced sign of PAD: class 4. Occurs at night when the patient is supine and arterial blood flow is so poor that gravity is needed to get blood to the foot

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25
What is the landmark category on the Rutherford classification system? What does it signify?
4: ischemic rest pain. Patient has limb-threatening ischemia!
26
What is Buerger's sign?
PE sign of advanced chronic ischemia. - Affected foot turns pale when elevated 1-2 min - Once patient dangles the foot down, it becomes ruborous like a cooked lobster (reactive hyperemia)
27
What is the differential of ischemic rest pain?
Severe PAD Diabetic neuropathy night cramps gout
28
What physical exam findings support PAD?
``` Pulse deficit Calf atrophy Hair loss Sweat gland atrophy (dry skin) Shiny skin Ulcers Cap refill > 2 sec ```
29
What is the most common muscle group affected by PAD, and in what artery is the atherosclerosis?
Calf muscles | Superficial femoral artery
30
What is the most common site of arterial emboli?
Common femoral artery
31
What is dependent rubor?
Dermal arterioles and capillaries don't constrict with increased hydrostatic pressure, vasodilation which results in pooling of blood in the foot when it is in a dependent position
32
What other diseases besides PAD can cause claudication?
Buerger's disease, vasculitis and entrapment of popliteal artery
33
What condition is associated with claudication in the UE?
Subclavian steal: atherosclerotic plaque narrows the subclavian, causing retrograde flow in the vertebral artery during arm exercise
34
How does location of muscle affected correlate with location of disease in PAD?
Muscle groups affected are generally supplied by arteries one level above
35
What is Leriche syndrome?
Chronic, slowly developing occlusion of infrarenal aorta, usually smokers: 1. Buttock/thigh claudication 2. Absent femoral pulses 3. Impotence
36
When PAD is suspected, what is the best next step?
1. Ankle brachial index | 2. Arterial duplex scan
37
How do we define PAD in terms of ABI?
ABI < 0.9 = PAD | Severe disease = < 0.4
38
If someone has PAD given their ABI, what is the next diagnostic step for someone whom an intervention is being planned?
CT angiogram or MR angiogram
39
What is the risk of limb loss for patients with ischemic rest pain in the foot?
50% that patient will have limb loss at one year without intervention
40
What signs/symptoms are considered limb threatening PAD?
Ischemic rest pain Nonhealing ulcer Gangrene
41
What is the initial management of claudication?
Medical management: - Smoking cessation - Exercise - Control HTN/DM - Statin - Aspirin
42
What drugs are approved for PAD?
Cilostazol: inhibits platelet aggregation, a vasodilator
43
Are statins indicated for PAD?
Yes, stabilize plaques and reduce risk of stroke and MI
44
Is aspirin indicated for PAD?
Yes
45
What are invasive therapeutic options for PAD?
Endovascular angioplasty / stenting and open surgical technique
46
Is there a role for invasive intervention in asymptomatic PAD?
No
47
Which patients with PAD should skip medical management and go straight to invasive approach?
Rutherford class 4-6, or ischemic rest pain or higher, since limb loss risk is significantly higher
48
What is the main cause of mortality in patients with PAD?
MI | Stroke
49
How can we tell dependent rubor of rest pain vs. cellulitis?
Raise the foot: - Ischemia: red skin is cool to the touch and upon elevation, rubor will disappear and foot will be pale - Cellulitis: red skin is warm and red color will persist
50
Is an ABI of 1.0 normal for a diabetic patient? Why or why not?
Diabetics may have falsely elevated ABI (>1.2) because they can develop Monkeberg's arteriolosclerosis causing calcification of the medial layer of the artery - causing it to become very rigid
51
Should a patient with claudication who is still smoking undergo an invasive procedure?
Many surgeons will not do surgery until they stop smoking because if they continue to smoke, PAD will progress
52
What is strongest risk factor for AAA?
smoking
53
Is diabetes a risk factor for AAA?
No
54
What is the limiting factor in detecting AAA in PE?
Obesity
55
Is there a role for AAA screening?
1 Physical exam and abdominal US one-time for men 65-75 who have had any smoking history 2 First degree relatives with AAA should be screened at age 60
56
If AAA is found, how often should patient be screening?
3-4cm: yearly | 4-4.5cm: 2x year
57
Is AAA associated with aneurysms elsewhere? If so, where? How can we screen?
Yes, femoral and popliteal. Screen with duplex US
58
How can thoracic aneurysms present?
Dysphagia, hoarseness, dyspnea and UE edema
59
What is the normal diameter of the infrarenal aorta?
2. 0cm men | 1. 8cm women
60
What is the primary defect in AAA?
Degeneration of medial layer through degradation of elastin and collagen
61
At what diameter is infrarenal aorta considered to be aneurysmal?
Focal area that is 1.5x larger than diameter of non-aneurysmal artery above
62
What is average annual growth rate of AAA?
2-4mm/year
63
What can increase and decrease the growth rate of AAA?
Smoking: increase Diabetes: decrease use of BP meds: decrease
64
What is the role of matrix metalloproteinases in AAA?
Key for collagen turnover. Patients with AAA have abnormally high levels of MMP in aortic wall which weakens arterial wall and dilates aneurysm over time
65
How do statins effect MMPs?
Decrease their activity
66
Does family history increase risk of AAA?
Yes - 12x higher risk if first degree relatives have it.
67
If an AAA ruptures, where does it go?
Usually retroperitoneum and to left as IVC prevents going to right
68
What are risk factors for AAA rupture?
1 Poorly controlled BP 2 AAA size 3 COPD 4 female gender
69
What is first step in evaluation of patient with suspected ruptured AAA?
ABCs of management of unstable patient. | If not in resp failure: delay intubation until OR.
70
In patient with suspected ruptured AAA, what is the goal of fluid resuscitation?
Limited! Permissive hypotension to keep systolic BP > 70 with no more than 1L crystalloid. If resuscitate too much, exacerbate hemorrhage by diluting out coagulation factors and raising systolic BP
71
What imaging for suspected ruptured AAA in hemodynamically stable patient?
CT angiogram
72
What imaging for suspected ruptured AAA in hemodynamically unstable patient?
Directly to OR for exploratory laparotomy. | If patient has no pulsatile mass and time permitting, bedside abdominal US used to confirm AAA.
73
Once an AAA is discovered, what is the management for < 4.4cm, 4.5-5.5, >5.5 and enlarging >1cm/year or symptomatic?
3-4.4cm: annual US 4.5-5.5cm: US every 3 months > 5.5cm: Elective repair Enlarging >1cm/year or symptomatic: elective repair
74
Why wait until aneurysm 5.5cm for repair?
Low risk for aneurysm < 5.5cm, and high morbidity and mortality of open surgical aneurysm repair.
75
What are surgical options for asymptomatic AAA?
Open repair | Endovascular aneurysm repair
76
What is main source of preoperative morbidity and mortality after asymptomatic AAA repair?
MI
77
What are the surgical options for a patient with ruptured AAA?
open repair of EVAR
78
What makes AAA unsuitable for EVAR?
Enough space to deploy the stent between the takeoff and renal arteries and start of infrarenal aneurysm. If too short, cannot do it!
79
What is mortality if an AAA ruptures?
80-90%
80
What is main Achilles heel of EVAR for AAA?
Failure to fully exclude aortic aneurysm. Persistent arterial flow into aneurysm sac = endoleak, which can cause aneurysm to grow and eventually rupture. requires annual followup to see if endoleak is present!
81
How to monitor patients after EVAR AAA repair?
CTA @ 1 month and 1 year to look for endoleak, then yearly. | Can also use duplex US but it has decreased specificity.
82
What is the most common cause of mortality after AAA surgical repair?
MI
83
At what diameter is an aorta considered aneurysmal?
3cm
84
If a patient has stable vital signs with a ruptured AAA, what is the management?
1. CT to confirm diagnosis, determine if EVAR possible | 2. Urgent repair via open or EVAR
85
If a patient has unstable vital signs with a ruptured AAA, what is the management?
1. immediate transport for open repair | 2. Consider US if diagnosis of AAA in question
86
What is management for non-ruptured AAA, < 5.5cm and >5.5cm?
<5.5: observe | >5.5: open or EVAR
87
If a patient has post-op bloody diarrhea a few days after AAA repair, what to consider?
Colonic ischemia
88
If a patient has bloody diarrhea months after AAA repair, what to consider?
Aortoenteric fistula
89
What is the difference between acute and chronic limb ischemia?
Acute < 2 weeks | Chronic > 2 weeks
90
What is the defining feature of acute limb ischemia? How do most patients present?
pulselessness | most patients present with pain
91
What are the common etiologies of acute limb ischemia?
Thrombosis Embolus (cardioembolic most common) Acute aortic dissection Systemic shock
92
What are the 6 P's of acute limb ischemia?
pain, pallor, pulselessness, paresthesias, paralysis, poikilothermia (perishing cold)
93
What is the most ominous sign of the 6 P's in acute limb ischemia?
Paralysis
94
What is the most common cause of acute arterial emboli?
A fib
95
Why is it important to ask about past interventions for PAD?
Thrombosis of a previous graft is a frequent cause of ALI
96
Where in the arterial tree do cardiac emboli tend to lodge? Why?
Arterial bifurcations due to reduced diameter
97
What two ways can atherosclerosis in the periphery lead to acute limb ischemia?
1. Plaque buildup leading to progressive narrowing of an artery with low flow states 2. Intraplaque rupture with local hypercoaguability and hemorrhage
98
How long can muscle tissue withstand ischemia before irreversible damage occurs?
3 hours: starts to show irreversible cell damage | 6 hours: complete cell damage
99
How do we determine the severity of acute limb ischemia? What are most important prognostic factors?
- Clinically - Motor and sensory deficits most important prognostic factors - Doppler signal used to see if any arterial flow present
100
What are the adjunct tests to vascular physical exam for ALI?
1. Doppler US probe: mono, di and triphasic | 2. Duplex US scan to see blood flow direction and velocity
101
What does triphasic vs. biphasic vs. monophasic represent in a doppler probe for assessment of ALI?
Triphasic: normal: 1. Initial systolic flow 2. Early diastolic retrograde flow 3. Forward diastolic flow Biphasic: could be normal, may represent early disease Monophasic: abnormal: signify severe reduction in blood flow
102
Why is ABI not used for ALI?
Blood flow is so reduced that BP is not measurable: ABI has limited utility
103
What is the first imaging recommended for ALI? If patient needs revascularization immediately?
Duplex scanning If emergent, do contrast angiography in the OR.
104
What are the 3 most important initial management steps for ALI?
1. Heparin to reduce clot spread 2. Place limb in dependent position to improve flow 3. IV fluids to optimize perfusion via collaterals
105
What are the main therapeutic options for ALI?
- Endovascular or open surgical revascularization | - Heparin alone if patient only has mild ischemia
106
How do we treat suspected ALI with normal motor/sensory function (I) or sensory deficit only (IIa)?
Imaging --> catheter-directed thrombolysis Consider surgical intervention if proximal embolus suspected
107
How do we treat suspected ALI with sensory and motor deficit (IIb)?
Surgical intervention
108
How do we treat suspected ALI with anesthesia and paralysis (stage III)?
Amputation
109
What is preferred treatment for ALI due to cardioemboli proximal extremity or above inguinal ligament?
Surgical embolectomy
110
What is preferred treatment for ALI due to thrombus?
Catheter-directed thrombolysis because lesions usually smaller, in distal vessels, associated with atherosclerosis
111
When ALI progresses to irreversible tissue damage, why do we do amputation and not pursue revascularization?
Reperfusion syndrome: toxic byproducts released from damaged tissue into general circulation. Hyperkalemia, rhabdo, ARDS, DIC.
112
After revascularization, what must be monitored?
1 CPK and myoglobinuria for concern for reperfusion syndrome | 2 EKG: hyperkalemia
113
How do we treat rhabdomyolysis from reperfusion syndrome?
1. IV fluids - enhance renal perfusion | 2. Bicarb infusion to alkalinize urine
114
What are causes of ALI?
``` A fib Acute MI Trauma Thrombosis of aneurysm Hypercoaguable states ```
115
How long does catheter-directed thrombolysis take to complete?
24-48 hours
116
What may be easily mistaken for ALI? How can we prevent?
- Acute neurologic event: especially if ischemia led to significant paresthesias and muscle weakness. - Do careful motor/sensory exam in addition to vascular exam - Normal pulses + normal ABI = rule out ALI

Surgery Clerkship (16 decks)

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