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Surgery Clerkship > Vascular > Flashcards

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
Q

What is the landmark category on the Rutherford classification system? What does it signify?

A

4: ischemic rest pain. Patient has limb-threatening ischemia!

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26
Q

What is Buerger’s sign?

A

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)
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27
Q

What is the differential of ischemic rest pain?

A

Severe PAD
Diabetic neuropathy
night cramps
gout

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28
Q

What physical exam findings support PAD?

A 
Pulse deficit
Calf atrophy
Hair loss
Sweat gland atrophy (dry skin)
Shiny skin
Ulcers
Cap refill > 2 sec
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29
Q

What is the most common muscle group affected by PAD, and in what artery is the atherosclerosis?

A

Calf muscles

Superficial femoral artery

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30
Q

What is the most common site of arterial emboli?

A

Common femoral artery

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31
Q

What is dependent rubor?

A

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

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32
Q

What other diseases besides PAD can cause claudication?

A

Buerger’s disease, vasculitis and entrapment of popliteal artery

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33
Q

What condition is associated with claudication in the UE?

A

Subclavian steal: atherosclerotic plaque narrows the subclavian, causing retrograde flow in the vertebral artery during arm exercise

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34
Q

How does location of muscle affected correlate with location of disease in PAD?

A

Muscle groups affected are generally supplied by arteries one level above

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35
Q

What is Leriche syndrome?

A

Chronic, slowly developing occlusion of infrarenal aorta, usually smokers:

  1. Buttock/thigh claudication
  2. Absent femoral pulses
  3. Impotence
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36
Q

When PAD is suspected, what is the best next step?

A
  1. Ankle brachial index

2. Arterial duplex scan

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37
Q

How do we define PAD in terms of ABI?

A

ABI < 0.9 = PAD

Severe disease = < 0.4

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38
Q

If someone has PAD given their ABI, what is the next diagnostic step for someone whom an intervention is being planned?

A

CT angiogram or MR angiogram

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39
Q

What is the risk of limb loss for patients with ischemic rest pain in the foot?

A

50% that patient will have limb loss at one year without intervention

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40
Q

What signs/symptoms are considered limb threatening PAD?

A

Ischemic rest pain
Nonhealing ulcer
Gangrene

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41
Q

What is the initial management of claudication?

A

Medical management:

  • Smoking cessation
  • Exercise
  • Control HTN/DM
  • Statin
  • Aspirin
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42
Q

What drugs are approved for PAD?

A

Cilostazol: inhibits platelet aggregation, a vasodilator

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43
Q

Are statins indicated for PAD?

A

Yes, stabilize plaques and reduce risk of stroke and MI

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44
Q

Is aspirin indicated for PAD?

A

Yes

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45
Q

What are invasive therapeutic options for PAD?

A

Endovascular angioplasty / stenting and open surgical technique

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46
Q

Is there a role for invasive intervention in asymptomatic PAD?

A

No

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47
Q

Which patients with PAD should skip medical management and go straight to invasive approach?

A

Rutherford class 4-6, or ischemic rest pain or higher, since limb loss risk is significantly higher

48
Q

What is the main cause of mortality in patients with PAD?

A

MI

Stroke

49
Q

How can we tell dependent rubor of rest pain vs. cellulitis?

A

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
Q

Is an ABI of 1.0 normal for a diabetic patient? Why or why not?

A

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
Q

Should a patient with claudication who is still smoking undergo an invasive procedure?

A

Many surgeons will not do surgery until they stop smoking because if they continue to smoke, PAD will progress

52
Q

What is strongest risk factor for AAA?

A

smoking

53
Q

Is diabetes a risk factor for AAA?

A

No

54
Q

What is the limiting factor in detecting AAA in PE?

A

Obesity

55
Q

Is there a role for AAA screening?

A

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
Q

If AAA is found, how often should patient be screening?

A

3-4cm: yearly

4-4.5cm: 2x year

57
Q

Is AAA associated with aneurysms elsewhere? If so, where? How can we screen?

A

Yes, femoral and popliteal. Screen with duplex US

58
Q

How can thoracic aneurysms present?

A

Dysphagia, hoarseness, dyspnea and UE edema

59
Q

What is the normal diameter of the infrarenal aorta?

A
  1. 0cm men

1. 8cm women

60
Q

What is the primary defect in AAA?

A

Degeneration of medial layer through degradation of elastin and collagen

61
Q

At what diameter is infrarenal aorta considered to be aneurysmal?

A

Focal area that is 1.5x larger than diameter of non-aneurysmal artery above

62
Q

What is average annual growth rate of AAA?

A

2-4mm/year

63
Q

What can increase and decrease the growth rate of AAA?

A

Smoking: increase
Diabetes: decrease
use of BP meds: decrease

64
Q

What is the role of matrix metalloproteinases in AAA?

A

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
Q

How do statins effect MMPs?

A

Decrease their activity

66
Q

Does family history increase risk of AAA?

A

Yes - 12x higher risk if first degree relatives have it.

67
Q

If an AAA ruptures, where does it go?

A

Usually retroperitoneum and to left as IVC prevents going to right

68
Q

What are risk factors for AAA rupture?

A

1 Poorly controlled BP
2 AAA size
3 COPD
4 female gender

69
Q

What is first step in evaluation of patient with suspected ruptured AAA?

A

ABCs of management of unstable patient.

If not in resp failure: delay intubation until OR.

70
Q

In patient with suspected ruptured AAA, what is the goal of fluid resuscitation?

A

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
Q

What imaging for suspected ruptured AAA in hemodynamically stable patient?

A

CT angiogram

72
Q

What imaging for suspected ruptured AAA in hemodynamically unstable patient?

A

Directly to OR for exploratory laparotomy.

If patient has no pulsatile mass and time permitting, bedside abdominal US used to confirm AAA.

73
Q

Once an AAA is discovered, what is the management for < 4.4cm, 4.5-5.5, >5.5 and enlarging >1cm/year or symptomatic?

A

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
Q

Why wait until aneurysm 5.5cm for repair?

A

Low risk for aneurysm < 5.5cm, and high morbidity and mortality of open surgical aneurysm repair.

75
Q

What are surgical options for asymptomatic AAA?

A

Open repair

Endovascular aneurysm repair

76
Q

What is main source of preoperative morbidity and mortality after asymptomatic AAA repair?

A

MI

77
Q

What are the surgical options for a patient with ruptured AAA?

A

open repair of EVAR

78
Q

What makes AAA unsuitable for EVAR?

A

Enough space to deploy the stent between the takeoff and renal arteries and start of infrarenal aneurysm. If too short, cannot do it!

79
Q

What is mortality if an AAA ruptures?

A

80-90%

80
Q

What is main Achilles heel of EVAR for AAA?

A

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
Q

How to monitor patients after EVAR AAA repair?

A

CTA @ 1 month and 1 year to look for endoleak, then yearly.

Can also use duplex US but it has decreased specificity.

82
Q

What is the most common cause of mortality after AAA surgical repair?

A

MI

83
Q

At what diameter is an aorta considered aneurysmal?

A

3cm

84
Q

If a patient has stable vital signs with a ruptured AAA, what is the management?

A
  1. CT to confirm diagnosis, determine if EVAR possible

2. Urgent repair via open or EVAR

85
Q

If a patient has unstable vital signs with a ruptured AAA, what is the management?

A
  1. immediate transport for open repair

2. Consider US if diagnosis of AAA in question

86
Q

What is management for non-ruptured AAA, < 5.5cm and >5.5cm?

A

<5.5: observe

>5.5: open or EVAR

87
Q

If a patient has post-op bloody diarrhea a few days after AAA repair, what to consider?

A

Colonic ischemia

88
Q

If a patient has bloody diarrhea months after AAA repair, what to consider?

A

Aortoenteric fistula

89
Q

What is the difference between acute and chronic limb ischemia?

A

Acute < 2 weeks

Chronic > 2 weeks

90
Q

What is the defining feature of acute limb ischemia? How do most patients present?

A

pulselessness

most patients present with pain

91
Q

What are the common etiologies of acute limb ischemia?

A

Thrombosis
Embolus (cardioembolic most common)
Acute aortic dissection
Systemic shock

92
Q

What are the 6 P’s of acute limb ischemia?

A

pain, pallor, pulselessness, paresthesias, paralysis, poikilothermia (perishing cold)

93
Q

What is the most ominous sign of the 6 P’s in acute limb ischemia?

A

Paralysis

94
Q

What is the most common cause of acute arterial emboli?

A

A fib

95
Q

Why is it important to ask about past interventions for PAD?

A

Thrombosis of a previous graft is a frequent cause of ALI

96
Q

Where in the arterial tree do cardiac emboli tend to lodge? Why?

A

Arterial bifurcations due to reduced diameter

97
Q

What two ways can atherosclerosis in the periphery lead to acute limb ischemia?

A
  1. Plaque buildup leading to progressive narrowing of an artery with low flow states
  2. Intraplaque rupture with local hypercoaguability and hemorrhage
98
Q

How long can muscle tissue withstand ischemia before irreversible damage occurs?

A

3 hours: starts to show irreversible cell damage

6 hours: complete cell damage

99
Q

How do we determine the severity of acute limb ischemia? What are most important prognostic factors?

A
  • Clinically
  • Motor and sensory deficits most important prognostic factors
  • Doppler signal used to see if any arterial flow present
100
Q

What are the adjunct tests to vascular physical exam for ALI?

A
  1. Doppler US probe: mono, di and triphasic

2. Duplex US scan to see blood flow direction and velocity

101
Q

What does triphasic vs. biphasic vs. monophasic represent in a doppler probe for assessment of ALI?

A

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
Q

Why is ABI not used for ALI?

A

Blood flow is so reduced that BP is not measurable: ABI has limited utility

103
Q

What is the first imaging recommended for ALI? If patient needs revascularization immediately?

A

Duplex scanning

If emergent, do contrast angiography in the OR.

104
Q

What are the 3 most important initial management steps for ALI?

A
  1. Heparin to reduce clot spread
  2. Place limb in dependent position to improve flow
  3. IV fluids to optimize perfusion via collaterals
105
Q

What are the main therapeutic options for ALI?

A
  • Endovascular or open surgical revascularization

- Heparin alone if patient only has mild ischemia

106
Q

How do we treat suspected ALI with normal motor/sensory function (I) or sensory deficit only (IIa)?

A

Imaging –> catheter-directed thrombolysis

Consider surgical intervention if proximal embolus suspected

107
Q

How do we treat suspected ALI with sensory and motor deficit (IIb)?

A

Surgical intervention

108
Q

How do we treat suspected ALI with anesthesia and paralysis (stage III)?

A

Amputation

109
Q

What is preferred treatment for ALI due to cardioemboli proximal extremity or above inguinal ligament?

A

Surgical embolectomy

110
Q

What is preferred treatment for ALI due to thrombus?

A

Catheter-directed thrombolysis because lesions usually smaller, in distal vessels, associated with atherosclerosis

111
Q

When ALI progresses to irreversible tissue damage, why do we do amputation and not pursue revascularization?

A

Reperfusion syndrome: toxic byproducts released from damaged tissue into general circulation. Hyperkalemia, rhabdo, ARDS, DIC.

112
Q

After revascularization, what must be monitored?

A

1 CPK and myoglobinuria for concern for reperfusion syndrome

2 EKG: hyperkalemia

113
Q

How do we treat rhabdomyolysis from reperfusion syndrome?

A
  1. IV fluids - enhance renal perfusion

2. Bicarb infusion to alkalinize urine

114
Q

What are causes of ALI?

A 
A fib
Acute MI
Trauma
Thrombosis of aneurysm
Hypercoaguable states
115
Q

How long does catheter-directed thrombolysis take to complete?

A

24-48 hours

116
Q

What may be easily mistaken for ALI? How can we prevent?

A
  • 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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