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Comprehensive Prep > Chapter 27: Vascular > Flashcards

Chapter 27: Vascular Flashcards

1
Q

Most common congenital hyper coagulable disorders

A

Resistance to activated protein C (Leiden factor)

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2
Q

Most common acquired hyper coagulable disorder

A

Smoking

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3
Q

Atherosclerotic stages

  • 1st
  • 2nd
  • 3rd
A

1) Foam cells (macrophages have absorbed fat and lipids in the vessel wall)
2) Smooth muscle cell proliferation (caused by growth factors released from macrophages; results in wall injury)
3) Intimal disruption (from smooth muscle cell proliferation)

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4
Q

What stage of athersclerosis causes thrombus formation?

A

Third - intimal disruption: leads to exposure of collagen in vessel wall and eventual thrombus formation -> fibrous plaques then form in these areas with underlying atheromas

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5
Q

Risk factors for atherosclerosis

A

Smoking, HTN, hypercholesterolemia, DM, hereditary factors

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6
Q

3rd most common cause of death in the United States

A

Stroke

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7
Q

Most important risk factor for stroke

A

HTN

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8
Q

Most common site of stenosis in cerebrovascular disease

A

Carotid bifurcation

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9
Q

Type of flow from normal internal carotid artery

A

Continuous forward flow

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10
Q

1st branch off the internal carotid artery

A

Ophthalmic artery

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11
Q

Type of flow from external carotid artery

A

Triphasic flow

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12
Q

1st branch of the external carotid artery

A

Superior thyroid artery

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13
Q

Communication between the ICA and ECA

A

Ophthalmic artery (off ICA) and internal maxillary artery (off ECA)

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14
Q

Most commonly diseased intracranial artery

A

Middle cerebral artery

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15
Q

Most commonly from arterial embolization from the ICA (not thrombosis)
- Can also occur from a low-flow state through a severely stenotic lesion

A

Cerebral ischemic events

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16
Q

Lesion: mental status changes, release, slowing

A

Anterior cerebral artery events

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17
Q

Lesion: contralateral motor and speech (if dominant side); contralateral facial droop

A

Middle cerebral artery events

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18
Q

Lesion: vertigo, tinnitus, drop attacks, incoordination

A

Posterior cerebral artery events

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19
Q

Occlusion of the ophthalmic branch of the ICA (visual changes -> shade coming down over eyes); visual changes are transient

A

Amaurosis fugax

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20
Q

What do you see on ophthalmologic exam in amaurosis fugax?

A

Hollenhorst plaques

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21
Q

Treatment: carotid traumatic injury with major fixed deficit:

  • Occlusion
  • Nonocclusion
A
  • If occluded, do not repair -> can exacerbate injury with bleeding
  • If not occluded -> repair with carotid stent or open procedure
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22
Q

Indications for CEA

A

Symptomatic > 50% (one or more TIAs within preceding 6mos), asymptomatic > 60% (if otherwise good candidate)

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23
Q

When do you consider CEA in a recent completed stroke?

A

Wait 4-6 weeks and then perform CEA if it meets criteria (bleeding risk if performed earlier)

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24
Q

Indications for emergent CEA

A

May be of benefit with fluctuating neurologic symptoms or crescendo / evolving TIAs

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25
Q

When do you use a shunt during CEA?

A

Use a shunt during CEA from stump pressures < 50 or if contralateral side is tight

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26
Q

What side do you repair if the patient has equally tight carotid stenosis bilaterally during CEA?

A

Repair the dominant side first if the patient has equally tight carotid stenosis bilaterally

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27
Q

Complications from repair during CEA

A
  • Vagus nerve injury
  • Hypoglossal nerve injury
  • Glossopharyngeal nerve injury
  • Ansa cervicalis
  • Mandibular branch of facial nerve
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28
Q

Most common cranial nerve injury with CEA

A

Vagus nerve: secondary to vascular clamping during endarterectomy; patients get hoarseness (recurrent laryngeal nerve comes off vagus)

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29
Q

CEA complication: tongue deviates to the side of injury-> speech and mastication difficulty

A

Hypoglossal nerve injury

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30
Q

CEA complication: rare, occurs with really high carotid dissection -> causes difficulty swallowing

A

Glossopharyngeal nerve injury

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31
Q

CEA complication: innervation to strap muscles; no serious deficits

A

Ansa cervicalis

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32
Q

CEA complication: affects corner of mouth (smile)

A

Mandibular branch of facial nerve

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33
Q

Treatment: acute event immediately after CEA

A

Back to OR to check for flap or thrombosis

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34
Q

Pulsatile, bleeding mass after CEA

- Treatment?

A

Pseudoaneurysm

Tx: drape and prep before intubation, intubate, then repair

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35
Q

Why do 20% have hypertension following CEA?

A

Caused by injury to the carotid body

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36
Q

Tx: HTN following CEA

A

Nipride to avoid bleeding

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37
Q

Most common cause of non-stroke morbidity and mortality following CEA

A

Myocardial infarction

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38
Q

Restonosis rate after CEA

A

15%

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39
Q

Indications for carotid stenting

A

For high-risk patients (e.g. patients with previous CEA and restenosis, multiple medical comorbidities, previous neck XRT)

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40
Q

Pathway of the vertebrobasilar artery

A

Two vertebral arteries arise from the subclavian arteries and combine to form a single basilar artery; the basilar then splits into two posterior cerebral arteries

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41
Q

Tx: vertebrobasilar artery disease

A

PTA with stent

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42
Q

What causes vertebrobasilar artery disease?

A

Caused by atherosclerosis, spurs, band; get vertebrobasilar insufficiency

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43
Q

Symptoms: diplopia, vertigo, tinnitus, drop attacks, incoordination

A

Vertebrobasilar artery disease

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44
Q

Tx: vertebrobasilar artery disease

A

PTA with stent

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45
Q

Present as a painless neck mass, usually near bifurcation, neural crest cells; are extremely vascular

A

Carotid body tumors

Tx: resection

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46
Q

What are the aortic arch vessels?

A

Innominate artery (which branches into the right subclavian and right common carotid arteries), the left common carotid artery, and the left subclavian artery

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47
Q
  • Often asymptotic and picked up on routine CXR

- Can get compression of vertebra (back pain), RLN (voice changes), bronchi (dyspnea or PNA), or esophagus (dysphagia)

A

Ascending aortic aneurysm

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48
Q

Indications for repair in ascending aortic aneurysm

A

Acutely symptomatic, > 5.5 cm (with Marfan’s > 5.0cm), or rapid increase in size ( > 0.5 cm/yr)

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49
Q

Indications for repair of descending aortic aneurysm (also thoracoabdominal aneurysms)

A

If endovascular repair possible > 5.5 cm.

If open repair needed > 6.5cm

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50
Q

Risk of mortality or paraplegia endovascular repair vs open repair

A

Less with endovascular repair (2-3%) compared to open repair (20%)

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51
Q

How can you help prevent paraplegia with open repair?

A

Reimplant intercostal arteries below T8 to help prevent paraplegia with open repair

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52
Q

What is the difference between the Stanford classification and the DeBakey Classification?

A
  • Stanford: based on presence or absence of involvement of ascending aorta
  • DeBakey: based on the site of tear and extent of dissection
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53
Q

Stanford classification: Class A

A

Any ascending aortic involvement

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54
Q

Stanford classification: class B

A

Descending aortic involvement only

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55
Q

Type I DeBakey

A

Ascending and descending

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56
Q

Type II DeBakey

A

Ascending only

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57
Q

Type III DeBakey

A

Descending only

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58
Q

Where do most dissections start?

A

In the ascending aorta

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59
Q

What can aortic dissection mimic?

A

Myocardial infarction

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60
Q

Symptoms: tearing like chest pain, can have unequal pulses (or BP) in upper extremities

A

Aortic dissection

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61
Q

What is present in 95% of patients with aortic dissection?

A

95% of patients have severe HTN at presentation

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62
Q

Risk factors for aortic dissection

A

Marfan’s syndrome, previous aneurysm, atherosclerosis

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63
Q

Where does aortic dissection occur?

A

Dissection occurs in the medial layer of blood vessel wall

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64
Q

Incidence of aortic insufficiency in aortic dissection

A

Aortic insufficiency: occurs in 70%, caused by annular dilatation or when aortic valve cusp is sheared off

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65
Q

What arteries are at risk in aortic dissection?

A

Can also have occlusion of the coronary arteries and major aortic branches

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66
Q

What is usually the cause of death in aortic dissection?

A

Death with ascending aortic dissections usually secondary to cardiac failure form aortic insufficiency, cardiac tamponade or rupture

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67
Q

Medical treatment initially for aortic dissections

A

Control BP with IV beta-blockers (e.g. esmolol) and Nipride

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68
Q

When to operate on ascending aortic dissections?

A

Operate on all ascending aortic dissections.

- Tx: need open repair; graft is placed to eliminate flow to the false lumen

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69
Q

When to operate on descending aortic dissections?

A

Only operate on descending aortic dissections with visceral or extremity ischemia or if contained rupture
- Tx: Endograft or open repair; can also just place fenestrations in the dissection flap to restore blood flow to viscera or extremity if ischemia is the problem.

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70
Q

Follow up for surgery for aortic dissection

A

Follow these patients with lifetime serial scans (MRI to decrease radiation exposure)

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71
Q

Why do people status post aortic dissection repair need lifetime follow up?

A

30% eventually get aneurysm formation requiring surgery

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72
Q

Post op complications for thoracic aortic surgery

A

MI, renal failure, paraplegia (descending thoracic aortic surgery)

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73
Q

Why is paraplegia a risk in aortic dissection repair?

A

Paraplegia is caused by spinal cord ischemia due to occlusion of intercostal arteries and artery of Adamkiewicz that occurs with descending thoracic aortic surgery

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74
Q

What causes AAA?

A

Results from degeneration of the medial layer

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75
Q

Leading cause of death in AAA

A

Rupture: leading cause of death without an operation

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76
Q

Symptoms: back or abdominal pain, can have profound hypotension

A

Rupture

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77
Q

Where is AAA most likely to rupture?

A

Most likely to rupture on left posterolateral wall, 2-4 cm below renals

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78
Q

When is AAA more likely to rupture?

A

More likely to rupture in the presence of diastolic HTN or COPD (thought to be predictors of expansion)

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79
Q

Rate of mortality with rupture of AAA if patient reaches hospital alive

A

50% mortality rate with rupture if patient reaches hospital alive

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80
Q

Indications for surgical repair of AAA

A

Repair if symptomatic, > 5.5 cm, or growth > 0.5 cm/yr

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81
Q

When do you reimplant the inferior mesenteric artery in surgical repair of ruptured AAA?

A

Reimplant IMA if back pressures

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82
Q

What arteries need ligation in ruptured AAA repair?

A

Ligate bleeding lumbar arteries

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83
Q

What artery needs ensured flow in aorto-bifemoral repair instead of straight tube graft in ruptured AAA repair?

A

If performing an aorto-bifemoral repair: ensure flow to at least one internal iliac artery (hypogastric artery) to avoid vasculogenic impotence

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84
Q

Graft used for repair of AAAs

A

Usually use a straight tube Dacron graft for repair of AAAs

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85
Q

Complications of AAA repair

A

Major vein injury with proximal cross-clamp. Impotence. MI. Renal failure. Graft infection. Pseudo aneurysm. Atherosclerotic occlusion. Diarrhea.

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86
Q

AAA complication: major vein injury with proximal cross-clamp

A

Retro-aortic left renal vein

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87
Q

AAA complication: impotence

A

In 1/3 secondary to disruption of autonomic nerves and blood flow to the pelvis

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88
Q

Rate of mortality with elective AAA repair

A

5% mortality with elective repair

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89
Q

1 cause of acute death after surgery

A

MI

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90
Q

1 cause of late death after surgery

A

Renal failure

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91
Q

Risk factors for mortality in AAA repair

A

Creatinine > 1.8 (#1), CHF, EKG ischemia, pulmonary dysfunction, older age, females

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92
Q

1 risk factor for mortality after AAA repair

A

Creatinine > 1.8

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93
Q

Graft infection rate s/p AAA repair

A

1%

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94
Q

Pseudoaneurysm formation s/p graft placement for AAA repair

A

1%

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95
Q

Most common later complication after aortic graft placement

A

Atherosclerotic occlusion

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96
Q

What is diarrhea (especially bloody) worrisome for after AAA repair?

A

Ischemic colitis

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97
Q

Why is ischemic colitis a possible complication in AAA repair?

A

Inferior mesenteric artery is often sacrificed with AAA repair and can cause ischemia (most commonly left colon)

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98
Q

Dx: ischemic colitis s/p AAA repair

A

Endoscopy or abdominal CT: middle and distal rectum are spared from ischemia (middle and inferior rectal arteries are branches off the internal iliac artery)

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99
Q

When do you go to OR for ischemic colitis s/p AAA repair?

A

If patient has peritoneal signs, mucosa is black on endoscopy, or part of the colon looks dead on CT scan -> take to OR for colectomy and colostomy placement

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100
Q

AAA: ideal criteria for endovascular repair:

  • Neck length
  • Neck diameter
  • Neck angulation
  • Common iliac artery length
  • Common iliac artery diameter
  • Other
A
  • Neck length: > 15mm
  • Neck diameter: 20-30mm
  • Neck angulation: 10mm
  • Common iliac artery diameter: 8-18mm
  • Other: non-tortuous, noncalcified iliac arteries, lack of neck thrombus
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101
Q

AAA repair: failure site -> Type 1 endoleak

A

Proximal or distal graft attachment sites

Tx: extension cuffs

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102
Q

AAA repair: failure site -> Type 2 endoleak

A

Collaterals (eg patent lumbar, IMA, intercostals, accessory renal)

Tx: observe most, percutaneous coil embolization if pressurizing aneurysm

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103
Q

AAA repair: failure site -> Type 3 endoleak

A

Overlap sites when using multiple grafts or fabric tear

Tx: Secondary endograft to cover overlap site or tear

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104
Q

AAA repair: failure site -> Type 4 endoleak

A

Graft wall porosity or suture holes

Tx: Observe, can place nonporous stent if that fails

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105
Q

AAA repair: failure site -> Type 5 endoleak (endotension)

A

Expansion of aneurysm without evidence of leak

Tx: repeat EVAR or open repair

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106
Q
  • Occurs in 10% of patients with AAA; males

- Weight loss, increased ESR, thickened rim above calcifications on CT scan

A

Inflammatory aneurysms

  • Not secondary to infection: just an inflammatory process
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107
Q

Anatomical problems to consider in inflammatory aneurysms

A
  • Can get adhesions to the 3rd and 4th portion of the duodenum
  • Ureteral entrapment in 25%
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108
Q

How do you prevent ureteral injury (25%) in repair of inflammatory aneurysms?

A

May need to place preoperative ureteral stents to help avoid injury.

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109
Q

Treatment: inflammatory aneurysm

A

Inflammatory process resolves after aortic graft placement

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110
Q

Cause of mycotic aneurysms

A 
#1 Salmonella
#2 Staphylococcus
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111
Q
  • Pain, fevers, positive blood cultures in 50%

- Periaortic fluid, gas, retroperitoneal soft tissue edema, lymphadenopathy

A

Mycotic aneurysms

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112
Q

Treatment: mycotic aneurysms

A

Usually need extra-anatomic bypass (axillary-femoral with femoral-to-femoral crossover) and resection of infrarenal abdominal aorta to clear infection

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113
Q

Causes of aortic graft infections

A 
#1 Staphylococcus
#2 E. coli
Blood cultures negative in many patients
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114
Q

What are aortic graft infections most common in?

A

More common with grafts going to the groin (e.g., aorto-bifemoral grafts)

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115
Q

Treatment: aortic graft infections

A

Bypass thru non-contaminated field (e.g. axillary-femoral bypass with femoral-to-femoral crossover) and then resect the infected graft

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116
Q
  • Usually occurs > 6 months after abdominal aortic surgery

- Herald bleed with hematemesis, then blood per rectum

A

Aortoenteric fistula

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117
Q

Where does the graft erode in aortoenteric fistula?

A

Graft erodes into 3rd or 4th portion of duodenum near proximal suture line

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118
Q

Standard treatment for an infected aortic valvular prosthesis

A

An axillobifemoral bypass is performed first. This is followed a few days later by removal of the infected aortic prosthesis and careful oversewing of the aortic stump as illustrated

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119
Q

Components of anterior leg compartment

A

Deep peroneal nerve (dorsiflexion, sensation between 1st and 2nd toes), anterior tibial artery

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120
Q

Components of lateral leg compartment

A

Superficial peroneal nerve (eversion, lateral foot sensation)

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121
Q

Components of deep posterior leg compartment

A

Tibial nerve (plantar flexion), posterior tibial artery, peroneal artery

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122
Q

Components of superficial posterior leg compartment

A

Sural nerve

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123
Q

Signs of PAD

A

Pallor, dependent rubor, hair loss, slow capillary refill

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124
Q

1 preventative agent for atherosclerosis

A

Statin drugs (lovastatin)

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125
Q

Can increase risk of atherosclerosis.

- Tx: folate and B12

A

Homocystinuria

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126
Q

How can you remember the symptoms associated with the level of occlusion in PAD?

A

Symptoms occur one level below occlusion

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127
Q

What can mimic claudication?

A

Lumbar stenosis

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128
Q

What can mimic rest pain in PAD?

A

Diabetic neuropathy

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129
Q
  • No femoral pulses
  • Buttock or thigh claudication
  • Impotence (from decreased flow in the internal iliacs)
A

Leriche syndrome

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130
Q

Where is the lesion in Leriche syndrome?

A

Lesion at aortic bifurcation or above

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131
Q

Treatment: Leriche syndrome

A

Aorto-bifemoral bypass graft

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132
Q

Most common atherosclerotic occlusion in the lower extremities

A

Hunter’s canal (distal superficial femoral artery exits here)

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133
Q

What muscle covers Hunter’s canal?

A

Sartorius muscle

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134
Q

What forms collateral circulation?

A

Forms form abnormal pressure gradients

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135
Q

Collateral circulation of circumflex iliacs

A

Circumflex iliacs to subcostals

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136
Q

Collateral circulation of circumflex femoral arteries

A

Circumflex femoral arteries to gluteal arteries

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137
Q

Collateral circulation around the knee

A

Geniculate arteries

138
Q

Budding from preexisting vessels; angiogenin involved

A

Postnatal angiogenesis

139
Q

Why can ABIs be very inaccurate in patients with diabetes?

A

Secondary to incompressibility of vessels; often have to go off Doppler waveforms in these patients

140
Q

How does walking affect the ABI?

A

In patients with claudication, the ABI in the extremity drops with walking

141
Q

When is arteriogram indicated in PAD?

A

If PVRs suggest significant disease - can also at times treat the patient with percutaneous intervention; gold standard for vascular imaging.

142
Q

Surgical indications for PAD

A

Rest pain, ulceration or gangrene, lifestyle limitation, atheromatous embolization

143
Q

How do you prevent vasculogenic impotence and pelvic ischemia during repair of aortoiliac occlusive disease?

A

Need to ensure flow to at least 1 internal iliac artery (hypogastric artery; want to see good back-bleeding from at least 1 of the arteries, otherwise need a bypass to an internal iliac artery) when performing aorto-bifemoral repair

144
Q

Treatment for isolated iliac lesions

A

PTA with stent 1st choice; if that fails, consider femoral-to-femoral crossover

145
Q
  • 75% 5-year potency

- improved patency with surgery for claudication as opposed to limb salvage

A

Femoropopliteal grafts

146
Q

Popliteal artery exposure below the knee:

  • Posterior muscle
  • Anterior muscle
A

Posterior muscle: gastrocnemius

Anterior muscle: popliteus

147
Q

Arteries useful in femoral-distal grafts

A

Peroneal, anterior tibial, or posterior tibial artery

148
Q

Rate of patency of femoral-distal grafts

A

50% 5-year patency; patency not influenced by level of distal anastomosis

149
Q

Why are distal lesions more limb threatening?

A

Because of lack of collaterals

150
Q

When are bypasses to distal vessels usually performed?

A

Usually used only for limb salvage

151
Q

If you are going to perform distal bypass on the leg, what do you need to ensure?

A

Bypassed vessel needs to have run-off below the ankle for this to be successful

152
Q

Dx: early swelling following lower extremity bypass

A

Reperfusion injury and compartment syndrome

Tx: fasciotomies

153
Q

Dx: late swelling following lower extremity bypass

A

DVT

Dx: US
Tx: heparin, coumadin

154
Q

Complications of reperfusion of ischemic tissue

A

Compartment syndrome, lactic acidosis, hyperkalemia, myoglobinuria

155
Q

1 cause of early failure of reversed saphenous vein grafts

A

Technical problem

156
Q

1 cause of late failure of reversed saphenous vein grafts

A

Atherosclerosis

157
Q

Noninfectious, can allow to autoamputate if small or just toes.

A

Dry gangrene

158
Q

Management of dry gangrene

A
  • Large lesions should be amputated

- See if patient has a correctable vascular lesion

159
Q

Infectious, need to remove infected necrotic material ; antibiotics

A

Wet gangrene

160
Q
  • At metatarsal heads

- Diabetics, can have osteomyelitis

A

Mal perforans ulcer

161
Q

MC’ly involved joint in mal performs ulcer

A

2nd MTP joint most common

162
Q

Tx: mal perforans ulcer

A

Non-weightbearing, debridement of metatarsal head (need to remove cartilage), antibiotics; assess need for revascularization

163
Q

What causes compartment syndrome?

A

Is caused by reperfusion injury to the extremity (mediated by PMNs; occurs with cessation of blood flow to extremity and repercussion > 4-6 hours later).

164
Q

Symptoms of compartment syndrome

A

Pain with passive motion; extremity feels tight and swollen

165
Q

Where is compartment syndrome most likely to occur?

A

Most likely to occur in the anterior compartment of leg (get foot drop)

166
Q

Dx / Tx: compartment syndrome

A

Dx: often based on clinical suspicion; compartment pressure > 20 - 30 mmHg abnormal

Tx: fasciotomies (get all 4 compartments if in lower leg) -> leave open 5-10 days

167
Q
  • Most present with mild intermittent claudication

- Men, 40s, loss of pulses with plantar flexion

A

Popliteal entrapment syndrome

168
Q

What leads to popliteal entrapment syndrome?

A

Have medial deviation of artery around medial head of gastrocnemius muscle

169
Q

Tx: popliteal entrapment syndrome

A

Resection of medial head of gastrocnemius muscle; may need arterial reconstruction

170
Q
  • Men, 40s, popliteral fossa most common area

- Symptoms: intermittent claudication, changes in symptoms with knee flexion / extension

A

Adventitial cystic disease

171
Q

Why is adventitial cystic disease most often bilateral?

A

Ganglia originate from adjacent joint capsule or tendon sheath

172
Q

Dx / Tx: adventitial cystic disease

A

Dx: angiogram

Tx: resection of cyst; vein graft if the vessel is occluded

173
Q

What are arterial autografts?

A

Radial artery grafts for CABG, IMA from CABG

174
Q

Rate of mortality within 3 years for leg amputation

A

50% mortality

175
Q

BKA:

  • ___% heal
  • ___% walk again
  • ___% mortality
A

80% heal
70% walk again
5% mortality

176
Q

AKA:

  • ___% heal
  • ___% walk again
  • ___% mortality
A

90% heal
30% walk again
10% mortality

177
Q

Indications for emergency amputation

A

Systemic complications or extensive infection

178
Q

Embolism or Thrombosis?

  • Arrhythmia
  • No prior claudication or rest pain
  • Normal contralateral pulses
  • No physical findings of chronic limb ischemia
A

Embolism

179
Q

Embolism or thrombosis?

  • No arrhythmia
  • History of claudication or rest pain
  • Contralateral pulses absent
  • Physical findings of chronic limb ischemia
A

Thrombosis

180
Q
  • Usually do not have collaterals, signs of chronic limb ischemia, or history of claudication with emboli (do have collaterals with thrombosis)
A

Acute arterial emboli

181
Q

Contralateral leg in acute arterial emboli

A

Contralateral leg usually has no chronic signs of ischemia and pulses are usually normal

182
Q

Symptoms: pain, paresthesia, poikilothermia, paralysis

A

Acute arterial emboli

183
Q

Extremity ischemia evolution in acute arterial emboli

A

Pallor (white) -> cyanosis (blue) -> marbling

184
Q

MCC acute arterial emboli

A

Atrial fibrillaiton

185
Q

Common causes of acute arterial emboli

A

A fib (MCC), recent MI with LV thrombus, myxoma, aorto-iliac disease

186
Q

MC site of peripheral obstruction from emboli

A

Common femoral artery

187
Q

Tx: acute arterial emboli

A

Embolectomy usual; need to get pulses back; post op angiogram
- Consider fasciotomy is ischemia > 4-6 hours

188
Q

When do you consider fasciotomy in acute arterial emboli?

A

If ischemia > 4-6 hours

189
Q

Treatment possibility in aortoiliac emboli (loss of both femoral pulses)

A

Can be treated with bilateral femoral artery cutdown and bilateral embolectomies

190
Q

Cholesterol clefts that can lodge in small arteries

A

Atheroma embolism

191
Q

Most common site of atheroma embolization

A

Renals

192
Q

Flaking atherosclerotic emboli off abdominal aorta or branches
- Patients typically have good distal pules

A

Blue toe syndrome

193
Q

MC source of blue toe syndrome

A

Aortoiliac disease

194
Q

Dx: atheroma embolism

A

Chest/abdomen/pelvis CT scan (look for aneurysmal source) and ECHO (clot or myxoma in heart)

195
Q

Tx: atheroma embolism

A

May need aneurysm repair or arterial exclusion with bypass

196
Q

Do patients with acute arterial thrombosis usually have arrhythmia?

A

No. These patients usually do not have arrhythmias.

197
Q

What is the usually history in acute arterial thrombosis?

A

Do have a history of claudication and have signs of chronic limb ischemia and poor pulses in the contralateral leg.

198
Q

Tx: acute arterial thrombosis

A

Threatened limb (loss of sensation or motor function) -> give heparin and go to OR for thrombectomy

If limb is not threatened: angiography for thrombolytics

199
Q

Treatment: thrombosis of PTFE graft

A

Thrombolytics and anticoagulation; if limb threatened -> OR for thrombectomy

200
Q

Where does the right renal artery run?

A

Posterior to IVC

201
Q

Rate of accessory renal arteries in humans

A

Accessory renal arteries in 25%

202
Q

Bruits. Diastolic blood pressure > 115, HTN, in children or premenopausal women, HTN resistant to drug therapy.

A

Renovascular HTN (renal artery stenosis)

203
Q

Renovascular HTN:

  • Left side
  • Proximal 1/3
  • Men
A

Renal atherosclerosis

204
Q

Renovascular HTN:

  • Right side
  • Distal 1/3
  • Women
A

Fibromuscular dysplasia

205
Q

Dx: renovascular HTN (renal atherosclerosis, fibromuscular dysplasia)

A

Angiogram

206
Q

Tx: renovascular HTN (renal atherosclerosis, fibromuscular dysplasia)

A

PTA (percutaneous transluminal angioplasty); place stent if due to atherosclerotic disease

207
Q

Indications for nephrectomy with renal HTN

A

Atrophic kidney

208
Q

Occlusive disease in the upper extremity: why are proximal lesions usually asymptomatic?

A

Secondary to increased collaterals

209
Q

Most common site of upper extremity stenosis

A

Subclavian artery

210
Q

Tx: occlusive disease of the upper extremity

A

PTA with stent; common carotid to subclavian artery bypass if that fails.

211
Q

Proximal subclavian artery stenosis resulting in reversal of flow through ipsilateral vertebral artery into the subclavian artery

A

Subclavian steal syndrome

212
Q

When do you operate in subclavian steal syndrome?

A

Operate with limb or neurologic symptoms (usually vertebrabasilar symptoms)

213
Q

Tx: subclavian steal syndrome

A

PTA with stent to subclavian artery, common carotid to subclavian artery bypass if that fails.

214
Q

Course of the subclavian vein

A

Passes over the first rib anterior to the anterior scalene muscle, then behind clavicle

215
Q

Course of the brachial plexus and subclavian artery

A

Passes over the first rib posterior to the anterior scalene muscle and anterior to the middle scalene muscle

216
Q

General symptoms: back, neck, and/or arm pain / weakness / tingling (often worse with palpation / manipulation)

A

Thoracic outlet syndrome

217
Q

Dx: thoracic outlet syndrome

A

Cervical spine and chest MRI, duplex US (vascular etiology), electromyelogram (EMG; neurologic etiology)

218
Q

If neurologic or vascular involvement more common in thoracic outlet syndrome?

A

Neurologic involvement - much more common than vascular

219
Q

1 anatomic abnormality in thoracic outlet syndrome

A

Cervical rib

220
Q

1 cause of pain in thoracic outlet syndrome

A

Brachial plexus irritation

221
Q

How does the exam look in thoracic outlet syndrome?

A

Usually have normal neurologic exam; tapping can reproduce symptoms (Tinsel’s test)

222
Q

Most common nerve distribution causing pain in thoracic outlet syndrome

A

Ulnar nerve distribution (C8-T1) - inferior portion of brachial plexus

223
Q

Symptoms of ulnar nerve distribution involvement in thoracic outlet syndrome

A

Tricep muscle weakness and atrophy, weakness of intrinsic muscles of hand, weak wrist flexion.

224
Q

Tx: thoracic outlet syndrome

A

Cervical rib and 1st rib resection, divide anterior scalene muscle

225
Q

Usually presents as effort-induced thrombosis of subclavian vein (Paget-von Schrotter disease; baseball pitchers) - acutely painful, swollen, blue limb

A

Subclavian vein TOS

226
Q

What type of thrombosis is involved in subclavian vein TOS

A

Venous thrombosis is much more common than arterial

227
Q

Dx: subclavian vein causing TOS

A

Venography is the gold standard for diagnosis, but duplex US makes the diagnosis and is quicker to get.

228
Q

Rate of thoracic outlet problem in subclavian vein problem causing TOS

A

80% have associated thoracic outlet problem.

229
Q

Tx: subclavian vein TOS

A

Thrombolytics initially; repair at that admission (Cervical rib and 1st rib resection, divide anterior scalene)

230
Q

Least common cause of TOS

A

Subclavian artery

231
Q

What is the cause of subclavian artery involvement in TOS?

A

Compression usually secondary to anterior scalene hypertrophy (weight lifters)

232
Q

Symptoms: subclavian artery TOS

A

Hand pain from ischemia

233
Q

Test used to confirm subclavian artery TOS

A

Adson’s test: absent radial pulse with head turned to ipsilateral side

234
Q

Dx / Tx: subclavian artery TOS

A

Dx: duplex US or angiogram (gold standard)

Tx: surgery -> cervical rib and 1st rib resection, divide anterior scalene muscle; possible bypass graft if artery is too damaged or aneursymal

235
Q

Why can motor function be preserved in digits after prolonged hand ischemia?

A

Motor function can remain in digits after prolonged hand ischemia because motor groups are in the proximal forearm.

236
Q
  • Overall mortality 60%
  • Usually involve SMA
  • CT findings: vascular occlusion, bowel wall thickening, intramural gas, portal venous gas
A

Mesenteric ischemia

237
Q

MCC of visceral ischemia

A
  • Embolic occlusion: 50%
  • Thrombotic occlusion: 25%
  • Nonocclusive: 15%
  • Venous thrombosis: 5%
238
Q

MC location of SMA embolism

A

Most commonly occurs near origin of SMA

239
Q
  • Pain out of proportion to exam; pain usually of sudden onset; hematochezia and peritoneal signs are late findings
  • May have h/o a fib, endocarditis, recent MI, recent angiography
A

SMA embolism

240
Q

Dx / Tx: SMA embolism

A

Dx: angiogram or abdominal CT with IV contrast

Tx: embolectomy, resect infarcted bowel if present

241
Q

How do you expose the SMA?

A

Divide ligament of Treitz, SMA is to the right of this near the base of the transverse colon mesentery

242
Q
  • Often history of chronic problems (food fear, weight loss)
  • Possible history of vasculitis or hyper coagulable state
  • Symptoms: similar to embolism, may have developed some collaterals
A

SMA thrombosis

243
Q

Tx: SMA thrombosis

A

thrombectomy (open or catheter directed; thrombolytics may have a role) ; may need PTA with stent or open bypass after the vessel is opened for any residual stenosis; resection of infarcted bowel

244
Q
  • Usually short segments of intestine involved; bloody diarrhea, crampy abdominal pain
  • May have a history of vasculitis, hyper coagulable state, portal HTN
A

Mesenteric vein thrombosis

245
Q

Dx / Tx: mesenteric vein thrombosis

A

Dx: abdominal CT scan or angiogram with venous phase

Tx: heparin usual; resection of infarcted bowel if present

246
Q
  • Spasm, low-flow states, hypovolemia, hemoconcentration, digoxin -> final common pathway is low cardiac output to visceral vessels
  • Symptoms: bloody diarrhea, pain
A

Nonocclusive mesenteric ischemia

247
Q

Final common pathway of nonocclusive mesenteric ischemia

A

Low cardiac output to visceral vessels

248
Q

Risk factors of nonocclusive mesenteric ischemia

A

Prolonged shock, CHF, prolonged cardiopulmonary bypass

249
Q

What areas are most vulnerable to nonocclusive mesenteric ischemia?

A

Watershed areas (Griffith’s - splenic flexure and Sudak’s - upper rectum)

250
Q

Watershed area: splenic flexure

A

Griffith’s

251
Q

Watershed area: upper rectum

A

Sudak’s

252
Q

Tx: nonocclusive mesenteric ischemia

A

Volume resuscitation, catheter-directed nitroglycerin can increase visceral blood flow; also need to increase cardiac output (dobutamine); resection of infarcted bowel if present

253
Q
  • Causes celiac artery compression

- Bruit near epigastrium, chronic pain, weight loss, diarrhea

A

Median arcuate ligament syndrome

254
Q

Tx: median arcuate ligament syndrome

A

Transect median arcuate ligament; may need arterial reconstruction

255
Q

Weight loss secondary to food fear (visceral angina 30 minutes after meals)

A

Chronic mesenteric ischemia

256
Q

Dx: chronic mesenteric ischemia

A

Get lateral visceral vessel aortography to see origins of celiac and SMA

257
Q

Tx: chronic mesenteric ischemia

A

PTA and stent; bypass if that fails

258
Q

Important collateral between the SMA and celiac

A

Arc of Riolan

259
Q

Most common complication of aneurysms above the inguinal ligament

A

Rupture

260
Q

Most common complications of aneurysms below inguinal ligament

A

Thrombosis and emoli

261
Q

Risk factors for visceral artery aneurysms

A

Medial fibrodysplasia, portal HTN, arterial disruption secondary to inflammatory disease (eg, pancreatitis)

262
Q

Repair guidelines for visceral artery aneursyms

A

Repair all splanchnic artery aneurysms (>2cm) when diagnosed (50% risk for rupture) except splenic

263
Q

MC visceral aneurysm

  • More common in women
  • 2% risk of rupture
A

Splenic artery aneurysm

264
Q

When do you repair splenic artery aneurysms?

A

If symptomatic, if patient is pregnant, if occurs in women of childbearing age, or is > 3-4 cm

265
Q

Splenic artery aneurysm: what is concerning in pregnants?

A

High rate of pregnancy-related rupture -> usually in 3rd trimester

266
Q

Tx: visceral artery aneurysm

A

Covered stent (best); exclusion with bypass if that fails

267
Q

Treatment splenic artery aneurysms

A

Splenic artery aneurysms can just be ligated if open procedure is required (have good collaterals)

268
Q

When do you treat renal artery aneurysms?

A

> 1.5 cm

Tx: covered stent

269
Q

When do you treat iliac and femoral artery aneurysms?

A

Iliac: > 3.0 cm
Femoral: > 2.5 cm

Tx: covered stent

270
Q

Most common peripheral aneurysm

A

Popliteal artery aneurysm

271
Q
  • Leg exam reveals prominent popliteal pulses
  • 1/2 are bilateral
  • 1/2 have another aneurysm elsewhere (AAA, femoral, etc)
  • Most likely to get thrombosis or emboli with limb ischemia
  • Can also get leg pain from compression of adjacent structures
A

Popliteal artery aneurysm

272
Q

Dx: popliteal artery aneurysm

A

Ultrasound

273
Q

Surgical indications for repair of popliteal artery aneurysm

A

Symptomatic, > 2cm, or mycotic

274
Q

TX: popliteal artery aneurysm

A

Exclusion and bypass of all popliteal aneurysms; 25% have complication that requires amputation if not treated; covered stent not recommended for these

275
Q

Collection of blood in continuity with the arterial system but not enclosed by all 3 layers of the arterial wall

A

Pseudoaneurysm

276
Q

Treatment pseudo aneurysm if it occurs after percutaneous intervention

A

Ultrasound-guided compression with thrombin injection (surgical repair if flow remains in the pseudo aneurysm after thrombin injection)

277
Q

Treatment pseudo aneurysm if it occurs at a suture line early after surgery

A

Need surgical repair

278
Q

What do pseudo aneurysms that occur at suture lines late after surgery (months to years) suggest?

A

Suggests graft infection

279
Q
  • Young women; HTN if renal involved; headaches or stroke if carotids involved
  • String of beads appearance
A

Fibromuscular dysplasia

280
Q

Most commonly involved vessel in fibromuscular dysplasia

A

Renal artery, followed by carotid and iliac

281
Q

Most common variant of fibromuscular dysplasia

A

Medial fibrodysplasia

282
Q
  • young men, smokers

- severe rest pain with bilateral ulceration; gangrene of digits, especially fingers

A

Buerger’s disease

283
Q

What do you see on arteriogram of Buerger’s disease?

A

Corkscrew collaterals on angiogram and severe distal disease; normal arterial tree proximal to popliteal and brachial vessels (i.e., a small vessel disease)

284
Q

Treatment: Buerger’s disease

A

Stop smoking of will require continued amputations

285
Q

Cystic medial necrosis syndromes

A

Marfan’s, Ehlers-Danlos syndrome

286
Q

Fibrillin defect (connective tissue elastic fibers); marfanoid habitus, retinal detachment, aortic root dilatation

A

Marfan’s disease

287
Q
  • Many types of collagen defects are identified
  • Easy bruising, hypermobile joints; tendency for arterial rupture, especially abdominal vessels
  • Get aneurysms and dissections
A

Ehlers-Danlos syndrome

288
Q

Angiogram protocol for Ehlers Danlos syndrome

A

No angiograms -> risk of laceration to vessel

289
Q

What is important to consider in Ehlers Danlos syndrome cystic medial necrosis?

A

Often too difficult to repair and need ligation of vessels to control hemorrhage

290
Q
  • Women, age > 55, headache, fever, blurred vision (risk of blindness)
  • Inflammation of large vessels (aorta and branches)
  • Long segments of smooth stenosis alternating with segments of larger diameter
A

Temporal arteritis (large artery)

291
Q

What do you see on temporal artery biopsy in temporal arteritis?

A

Giant cell arteritis, granuloma

292
Q

Tx: temporal arteritis (large artery)

A

Steroids, bypass of large vessels if needed; no endarterectomy

293
Q
  • Weight loss, rash, arthralgias, HTN, kidney dysfunction
  • Get aneurysms that thromboses or rupture
  • Renals most commonly involved
A

Polarteritis nodosa (medium artery)

294
Q

What organ is most commonly involved in polyarteritis nods?

A

Renals

295
Q

Tx: polyarteritis nodosa (medium artery)

A

Steroids

296
Q
  • Children; febrile viral illness with erythematous mucosa and epidermis
  • Get aneurysms of coronary arteries and brachiocephalic vessels
  • Die from arrhythmias
A

Kawasaki’s disease (medium artery)

297
Q

What do people with Kawasaki’s die from?

A

Arrhythmias

298
Q

Tx: Kawasaki disease

A

Steroids, possible CABG

299
Q
  • Often secondary to drug / tumor antigens

- Symptoms: rash (palpable purpura), fever, symptoms of end-organ dysfunction

A

Hypersensitivity angiitis (small artery)

300
Q

Tx: hypersensitivity angiitis (small artery)

A

Calcium channel blockers, pentoxifylline, stop offending agent

301
Q

Radiation arteritis:

  • Early
  • Late
  • Late late
A
  • Early: sloughing and thrombosis (obliterative endarteritis)
  • Late: (1-10 years) - fibrosis, scar, stenosis
  • Late late (3-30 years) - advanced atherosclerosis
302
Q
  • Young women

- Pallor -> cyanosis -> rubor

A

Raynaud’s disease

303
Q

Tx: Raynaud’s disease

A

Calcium channel blockers, warmth

304
Q

Joins femoral vein near groin; runs medially

A

Greater saphenous vein

305
Q

Why no clamps on the IVC?

A

Will tear

306
Q

Can be ligated near the IVC in emergencies because of collaterals (left gonadal vein, left adrenal vein); right renal vein does not have these collaterals

A

Left renal vein

307
Q

Most common failure of AV grafts for dialysis

A

Venous obstruction secondary to intimal hyperplasia

308
Q

Dialysis access grafts:

  • Radial artery to cephalic vein
  • Wait 6 weeks to use -> allows vein to mature
A

Cimino

309
Q

Dialysis access grafts

  • eg brachiocephalic loop graft
  • wait 6 weeks to allow fibrous scar to form
A

Interposition graft

310
Q

Two types of dialysis access graft

A

Cimino, interposition graft

311
Q
  • Usually secondary to trauma; can get peripheral arterial insufficiency, CHF, aneurysm, limb-length discrepancy
  • Most need repair -> lateral venous suture; arterial side may need patch or bypass graft; try to place interposing tissue so it does not recure
A

Acquired AV fistula

312
Q
  • Causes: smoking, obesity, low activity

- Tx: sclerotherapy

A

Varicose veins

313
Q
  • Secondary to venous valve incompetence (90%)

- Ulceration occurs above and posterior to malleoli

A

Venous ulcers

314
Q

Venous ulcers: size that often heal without surgery

A

Ulcers > 3cm often heal without surgery

315
Q

Tx: venous ulcers

A

Unna boot compression cures 90%

316
Q

What do you need to consider in the treatment of venous ulcers?

A

May need to ligate perforators or have vein stripping of greater saphenous vein

317
Q
  • Aching, swelling, night cramps, brawny edema, venous ulcers
  • Elevation brings relief
A

Venous insufficiency

318
Q

Tx: venous insufficiency

A

Leg wraps, ambulation with avoidance of long standing

319
Q

Treatment of venous ulcers: for severe symptoms or recurrent ulceration despite medical treatment

A

Greater saphenous vein stripping (for saphenofemoral valve incompetence) or removal or perforators (if just perforator valves are incompetent; stab avulsion technique)

320
Q

Nonbacterial inflammation

- Tx: NSAIDs, warm packs, ambulation

A

Superficial thrombophlebitis

321
Q
  • Pus fills vein; fever, increased WBCs, erythema, fluctuant; usually associated with infection following a peripheral IV
  • Tx: resect entire vein
A

Suppurative thrombophlebitis

322
Q

What is associated with migrating thrombophlebitis?

A

Pancreatic CA

323
Q

MOA: Sequential compression devices (SCDs)

A

Help prevent blood clots by decreasing venous stasis and increasing tPA release

324
Q

Why is the left leg 2x more involved than right in DVT?

A

Longer left iliac vein compressed by right iliac artery

325
Q

Tenderness, pallor (whiteness), edema

- Tx: heparin

A

Phlegmasia alba dolens

326
Q

IVC filter indications

A

Contraindication to anticoagulation; PE while on coumadin; free-floating ileofemoral thrombi; after pulmonary embolectomy

327
Q

Etiology of pulmonary embolism with filter in place

A

Comes from ovarian veins, inferior vena cava superior to filter, or from upper extremity via the superior vena cava

328
Q

Treatment: venous thrombosis with central line

A

Pull out central line if not needed, then heparin; can try to treat with systemic heparin or TPA down line if the access site is important

329
Q
  • Do not contain a basement membrane

- Not found in bone, muscle, tendon, cartilage, brain, or cornea

A

Lymphatics

330
Q

Are lymphatics valveless?

A

Deep lymphatics have valves

331
Q
  • Occurs when lymphatics are obstructed, too few in number, or nonfunctional
  • Leads to woody edema secondary to fibrosis in subcutaneous tissue (toes, feet, ankle, leg)
A

Lymphedema

332
Q

What are big problems in lymphedema?

A

Cellulitis and lymphangitis secondary to minor trauma are big problems

333
Q

Most common infection in lymphedema

A

Strep

334
Q

Laterality of congenital lymphedema

A

L > R

335
Q

Tx: lymphedema

A

Leg elevation, compression, antibiotics for infections

336
Q

Raised blue/red coloring; early metastases to lung

A

Lymphangiosarcoma

337
Q

Lymphangiosarcoma associated with breast axillary dissection and chronic lymphedema

A

Stewart-Treves syndrome

338
Q
  • Usually after dissection in the groin (e.g. after femoral to popliteal bypass)
  • Leakage of clear fluid
A

Lymphocele

339
Q

Tx: lymphocele

A

Percutaneous drainage (can try a couple of times); resection if that fails

340
Q

How can you identify the lymphatic channels supplying a lymphocele?

A

Can inject isosulfan blue dye into foot to identify the lymphatic channels supplying the lymphocele if having trouble locating.

Comprehensive Prep (45 decks)

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