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ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn > Chapter 27 - Vascular++ > Flashcards

Chapter 27 - Vascular++ Flashcards

1
Q

What is the most common congenital hypercoagulable disorder?

A

Resistance activated protein C (factor V) Leiden factor

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2
Q

What is most common acquired hypercoagulability disorder?

A

Smoking

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3
Q

What are the three stages of atherosclerosis?

A
  1. Foam cells - macrophages that have absorbed fat and lipids in the vessel wall.
  2. Smooth muscle cell proliferation - caused by growth factors (PDGF) released from macs; results in wall injury.
  3. Intimal disruption from smooth muscle cell proliferation - leads to exposure of collagen in the vessel wall and eventual thrombus formation - fibrous plaques then form in these areas with underlying atheromas
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4
Q

What are the risk factors for atherosclerosis?

A
  1. smoking - vascular mortality dec to nonsmoker if pt quits for 20 yrs; causes endothelial dysfx and thrombosis
  2. DM - distal dz, inc risk of ampx
  3. HTN - ctrl to prevent cardiac and CVA
  4. cholesterol - statin
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5
Q

Atherosclerosis is a disease of what part of the blood vessel?

A

Disease of intima (deposition occurs in innermost layer).

Vessel compromised at 40%.

Rupture of cap exposes thrombogenic LDL core.

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6
Q

Hypertension is a disease of what part of the blood Vessel?

A

Disease of the media (tension occurs in the muscular layer)

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7
Q

What is the most important risk factor for stroke in asymptomatic patients?

A

Hypertension

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8
Q

Where is the most common site for stenosis in the carotid arteries?

A

Bifurcation

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9
Q

The normal internal carotid artery has what type of flow?

A

Continuous forward flow (brain needs continuous perfusion)

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10
Q

The normal external carotid artery has what type of flow?

A

Triphasic flow (externals go to high pressure beds)

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11
Q

Where is the communication between the internal carotid artery and the external carotid artery?

A

Ophthalmic artery (first branch of ICA) and internal maxillary artery off ECA

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12
Q

What is the most commonly diseased intracranial artery?

A

Middle cerebral artery

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13
Q

What is the most common etiology of cerebral ischemic events?

A

Arterial embolization from the ICA. Heart is the second most common source of emboli.

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14
Q

Anterior cerebral artery events cause what?

A

Mental status changes, release, slowing

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15
Q

Middle cerebral artery events cause what?

A

Contralateral motor and speech loss; contralateral facial droop

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16
Q

What is amaurosis fugax?

A

Occlusion of the ophthalmic branch of the ICA causing painless visual changes - shade coming down over eyes; visual changes are transient. Can see Hollenhorst plaques on ophthalmologic exam.

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17
Q

What do you do with carotid traumatic injury with major fixed deficit?

A

If occluded do not repair-can exacerbate injury with bleeding. If not occluded-repair.

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18
Q

When do you consider a carotid endarterectomy?

A
  • Men w/ sx + >50% stenosis.
  • Women w/ sx + >70% stenosis.
  • Asx pt w/ >80 stenosis.
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19
Q

The patient has a recent completed stroke, when do you perform CEA?

A

4 to 6 weeks

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20
Q

When can an urgent CEA be of benefit?

A
  • When there are fluctuating neurologic symptoms - crescendo/evolving TIAs.
  • Between 3-14 days
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21
Q

When do you shunt during a CEA?

A

When the stump pressure is less than 50

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22
Q

What is the most common cranial nerve injury with a carotid endarterectomy?

A

Vagus nerve secondary to vascular clamping during endarterectomy. Patients get hoarseness.

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23
Q

What happens with a hypoglossal nerve injury during CEA?

A

Tongue deviation to the side of the injury - speech and mastication difficulty.

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24
Q

What happens with a glossopharyngeal nerve injury during a CEA?

A

Unlikely. Could occur with a really high carotid lesion. Causes difficulty swallowing.

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25
Q

What happens if you damage the Ansa cervicalis during a CEA?

A

Innervates strap muscles; no serious deficits

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26
Q

What happens if you damage the mandibular branch of the facial nerve during a CEA?

A

Affects corner of mouth (smile). Will get called in PACU for possible stroke, but is often transient stun 2/2 overzealous retraction at the mandible.

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27
Q

What do you do if there’s an acute cerebrovascular event immediately after a CEA?

A

Go back to the OR to check for flap or thrombosis

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28
Q

How do you detect a pseudoaneurysm after a CEA, and what do you do about it?

A

Pulsatile, bleeding mass after CEA. Draped and prepped before intubation, intubate, then repair

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29
Q

What percentage of patients have hypertension following a CEA and why?

A

20%. Caused by injury to carotid body. Treat with nipride to avoid bleeding.

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30
Q

What is the restenosis rate after a CEA?

A

15%

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31
Q

What are the symptoms of Vertebral artery disease, and what is the treatment?

A
  • Psx: Diplopia, dysarthria, vertigo, tinnitus, drop attacks, incoordination, binocular vision loss.
  • Dx: MRA vs arteriogram
  • Tx if sx, >1.5 cm aneurysm, >60% stenosis
  • Tx: PTA, VA transposition to SCA, endarterectomy, osteophyte resection, unroofing of transverse process foramina, resection of musculotendinous bands
    • V1: reconstruct
    • V2: bypass to V3
    • V4: endovascular
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32
Q

How do carotid body tumors present?

A

Painless neck mass, usually at the bifurcation, made up of neural crest cells. Treat all with resection.

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33
Q

How do you get a thoracic aortic injury, and what you do about it?

A

Deceleration injury. Dx: CTA. Tx: stable and contained (intimal tear only) - antihypertensives until systolic <100 and HR <100; unstable, intramural hematoma, pseudoaneurysm, rupture - intervention with stent-graft

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34
Q

What are ascending aortic aneurysms usually caused by?

A

Usually caused by connective tissue disorder; cystic medial necrosis most common abnormality - Marfan syndrome. Often asymptomatic and picked up on routine CXR. Can get compression of vertebral a, hoarse whisper, dyspnea, trouble swallowing.

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35
Q

Transverse aortic arch aneurysms from?

A

From atherosclerosis. Repair symptomatic, greater than 5.5 cm, greater than 5 cm if Marfan’s.

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36
Q

Descending aortic aneurysms etiology? Management?

A

From atherosclerosis. Repair if greater than 5.5 cm. Reimplant intercostal vessels below t8 to help prevent paraplegia.

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37
Q

Classifications of dissections?

A
  • Stanford:
    • A) Any ascending aortic involvement
    • B) Descending aortic involvement only
  • DeBakey:
    • I) Ascending and descending
    • II) Ascending only
    • III) Descending only
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38
Q

Where do most dissections start in the aorta?

A

Ascending aorta

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39
Q

What are symptoms of an aortic dissection?

A

Can mimic MI, Searing chest pain, unequal pulses or BP in upper extremities. 95% have severe hypertension.

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40
Q

What are the risk factors for aortic dissection?

A

Hypertension (medial disease), Marfan’s (cystic medial necrosis), Previous aortic coarctation repair, atherosclerosis, syphilis

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41
Q

What layer of the aorta does a dissection occur?

A

Media (association with hypertension)

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42
Q

Why does aortic insufficiency occur with aortic dissection?

A

Occurs in 70% with acute disease. Caused by annular dilatation or when aortic valve cusp is sheared off. Can also have occlusion of the coronaries and major aortic branches. Death from aortic insufficiency or tamponade.

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43
Q

What aortic dissections need operations?

A

All ascending aortic dissections. Descending aortic dissections with visceral, renal, or leg ischemia; persistent pain; large-size. Need to follow with lifetime serial CT scans; 30% will eventually get aneurysm formation requiring surgery (5.5 cm).

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44
Q

What are the most common postop complications for thoracic aorta surgery?

A

MI, renal failure, paraplegia due to occlusion of the intercostal arteries and artery of adamkiewicz during repair - prevent with lumbar drains.

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45
Q

How big is the normal aorta?

A

2 to 3 cm

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46
Q

What causes abdominal aortic aneurysms?

A

Most commonly due to atherosclerosis. Form from degeneration of the medial layer. Risk factors include hypertension, male gender, smoking, elderly age, and spinal cord injury.

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47
Q

What is the leading cause of death in AAA patients without an operation?

A

Rupture

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48
Q

What is the five-year rupture risk of a 5 cm AAA? What is the five-year rupture risk of an 8 cm AAA?

A

15 to 20%. 100%.

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49
Q

What is seen on the CT of a ruptured AAA?

A

Fluid in retroperitoneal space, extraluminal contrast

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50
Q

Where are AAA’s most likely to rupture?

A
  • Left posterior lateral wall, 2 to 4 cm below renals
  • Most likely in presence of diastolic HTN or COPD
  • 50% mortality with rupture
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51
Q

When do you need to re-implant the IMA?

A
  • When back pressures less than 40 MM HG, previous colonic surgery, stenosis at SMA, flow to left colon appears inadequate. Whenever possible.
  • No need if 0 backbleeding as vessel is occluded.
  • Ligate bleeding lumbar arteries.
  • Maintain flow to at least one internal iliac artery
  • 35% will suffer from some degree of colonic ischemia in ruptured AAA.
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52
Q

What major vein injury is common with AAA repair

A

Retroaortic renal vein with proximal cross-clamp

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53
Q

What is the mortality of an elective AAA repair?

A

5%

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54
Q

What is the number one cause of acute death after AAA surgery?

A

MI

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55
Q

What is the number one cause of late death after surgery for a AAA?

A

Renal failure

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56
Q

What is the rate of AAA repair graft infection?

A

1%

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57
Q

What is the risk of pseudoaneurysm after AAA graft placement?

A

1%

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58
Q

What is the most common late complication after aortic graft placement?

A

Atherosclerotic occlusion

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59
Q

What can cause ischemic colitis after a AAA repair?

A

The inferior mesenteric artery is often sacrificed

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60
Q

What is a type I endoleak?

A

Proximal or distal attachment zone 2.2 stent migration. Treat with proximal or distal extension cuff.

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61
Q

What is a type II endoleak?

A

Retrograde endoleak 2/2 patent lumbar, IMA, intercostals, accessory renal etc. Treat w/ percutaneous coil embolization

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62
Q

What is a type III endoleak?

A

Midgraft component disconnection 2/2 fabric tear. Treat with secondary Endograft

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63
Q

What is a type IV endoleak?

A

Graft wall porosity or suture holes. Treat with secondary stenting or observe.

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64
Q

What is a type V endoleak?

A

High intrasac pressure without leak shown. Secondary repair or open repair.

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65
Q

What is an inflammatory aneurysm?

A

Occurs in 10% of patients. Adhesions to the third and fourth portions of the duodenum. Ureteral entrapment in 25%. NOT secondary to infection. Assn w/ weight loss, increased ESR, thickened rim above calcifications on CT scan.

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66
Q

Mycotic aneurysms etiology? Symptoms? Imaging findings? Management?

A

Salmonella number one cause, staphylococcus number two. Psx: Pain, fevers, positive blood cultures. Img: Periaortic fluid/gas, retroperitoneal soft tissue edema, lymphadenopathy. Tx: Need extra-anatomic bypass and resection of infrarenal abdominal aorta to clear infection.

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67
Q

Aortic graft infections etiology? Imaging findings? Management?

A

Staphylococcus number one, E. coli number two. Img: See fluid, gas, thickening around graft. Tx: Resect graft and bypass through non-contaminated field. Blood cultures negative in many patients. More common with graphs going to groin.

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68
Q

Aortoenteric fistula timing? Symptoms? Location?

A

Usually occurs more than six months after surgery. Herald bleed with hematemesis, then blood per rectum. In third or fourth portion of duodenum near proximal suture line.

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69
Q

What is affected in the anterior leg compartment?

A

Deep peroneal nerve-dorsiflexion, sensation between first and second toes. Anterior tibial artery.

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70
Q

What is affected in the lateral leg compartment?

A

Superficial peroneal nerve-Eversion, lateral foot sensation

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71
Q

What is affected in the deep posterior leg compartment?

A
  • Tibial nerve-plantarflexion
  • Posterior tibial artery, peroneal artery
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72
Q

What is affected in the superficial posterior leg compartment?

A

Sural nerve

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73
Q

What are the signs of PVD?

A

Palor, hair loss, dependent rubor, abnormal nail growth, slow capillary refill. Most commonly due to atherosclerosis.

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74
Q

What is the number one prevention agent for atherosclerosis?

A

Statin drugs

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75
Q

Gluteal claudication pain is due to blockage of what artery?

A

Aorto iliac disease

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76
Q

Midthigh claudication is due to disease in what artery?

A

External iliac

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77
Q

Calf claudication is due to disease of what arteries?

A

Common femoral artery or proximal superficial femoral artery

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78
Q

Foot claudication is due to disease of what artery?

A

Distal superficial femoral artery or popliteal disease

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79
Q

What can mimic claudication?

A

Lumbar stenosis

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80
Q

What can mimic rest pain?

A

Diabetic neuropathy

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81
Q

What is Lerich syndrome?

A

No femoral pulses, gluteal or thigh claudication, erectile dysfunction. Lesion at aortic bifurcation or above.

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82
Q

Where is the most common atherosclerotic occlusion in the lower extremities?

A

Hunters canal-distal superficial femoral artery exits here. Sartorius muscle covers hunters canal

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83
Q

What is postnatal angiogenesis?

A

Budding from pre-existing vessels; AngioGenin involved

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84
Q

At what ABI do you get rest pain?

A

Less than .5

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85
Q

At what ABI do you get ulcers?

A

Less than .4. Ulcers usually start in toes

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86
Q

Why are ABI’s inaccurate in patients with diabetes?

A

Incompressible vessels

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87
Q

What are the surgical indications for PVD?

A

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

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88
Q

Aorto iliac occlusive disease management?

A

“Inflow disease” of younger smokers. Define w/ ABI. Reduce risk w/ aspirin and control of HTN, DM, smoking. Lower thresh-hold for intervention - PTA (short single lesions) vs surgery. Address before infra-inguinal lesions. In high-risk patients perform bilateral axillary femoral bypasses or an axillary femoral bypass with a femoral to femoral crtossover to stay out of the abdomen

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89
Q

What do you do with isolated iliac lesions?

A

Angioplasty with stent is first choice; if that fails perform aorto bifemoral repair or femoral to femoral crossover

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90
Q

What is the patency of femoropopliteal grafts?

A

75% for five years. Improved patency rate in patients with surgery for claudication as opposed to limb salvage

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91
Q

What is the patency of femoral distal grafts?

A

50% five-year patency; not influenced by level of distal anastomosis. Distal lesions more limb threatening because of what lack of collaterals. Bypasses distal usually used only for limb salvage.

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92
Q

What is a complication of femoral femoral crossover graft?

A

Vascular steal in donor leg

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93
Q

Swelling following lower extremity bypass caused by what?

A

One: DVT; two edema from reperfusion injury

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94
Q

What are the complications of reperfusion of ischemic tissue?

A

Lactic acidosis, hyperkalemia, myoglobinuria, compartment syndrome

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95
Q

What is the number one cause of late failure of reverse saphenous Vein grafts?

A

Atherosclerosis

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96
Q

What is the number one cause of early failure of reverse saphenous vein grafts?

A

Technical problem

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97
Q

What do you do with a patient with a heel ulceration to the bone?

A

Amputate

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98
Q

What is dry gangrene?

A

Noninfectious; can allow to auto amputate in toes. Amputate if a large lesion, see if patient has correctable vascular lesion

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99
Q

What is wet gangrene?

A

Infectious; amputation to remove infected necrotic material, antibiotics, surgical emergency

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100
Q

What is a mal perforans ulcer?

A
  • At metatarsal heads in DM pts w/ neuropathy
  • second MTP most common
  • can have OM - may need ray amputation
  • treat underlying DM and neuropathy
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101
Q

When do you use percutaneous transluminal angioplasty?

A

Excellent for common iliac lesions. Best for short stenoses. Intima usually ruptured and media stretched, pushes the plaque out. Requires passage of wire first

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102
Q

What do you do with a pseudoaneurysm after arteriography?

A
  • US Duplex to diagnose
  • Observe if <2 cm w/ US monitoring.
  • Thrombin injection with ultrasound guidance.
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103
Q

In what part of the leg is compartment syndrome most likely to occur?

A

Anterior compartment. Get footdrop. Pressures greater than 20 to 30 abnormal; consider fasciotomy - leave open for 5 to 10 days.

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104
Q

What is popliteal entrapment syndrome?

A
  • Most present with mild intermittent claudication, loss of pulses with plantarflexion, usually have medial deviation of artery around the medial head of gastrocnemus muscle.
  • Treatment is resection of medial head of gastrocnemius muscle. May need arterial reconstruction
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105
Q

What is adventitial cystic disease?

A
  • Popliteal most common area. Often bilateral-ganglia originate from adjacent joint capsule or tendon sheath.
  • Intermittent claudication. Changes in symptoms with knee flexion/extension.
  • Treat with vein graft if occluded; otherwise just resection of cyst
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106
Q

With a BKA, what percentage heal, what percentage walk again, what is the mortality?

A

80% heal, 70% walk again, 5% mortality

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107
Q

With an AKA, what percentage heal, what percent walk again, what is the mortality?

A

90% heal, 30% to walk again, 10% mortality

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108
Q

What are the signs of an acute arterial emboli?

A

No signs of chronic ischemia. contralateral leg usually pulses are normal. First pallor, then cyanosis, then marbling. Symptoms include pain, pallor, pulselessness, parasthesia, poillothermia, paralysis.

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109
Q

What is the most common cause of arterial emboli?

A

A fib

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110
Q

What are other causes of arterial emboli?

A

LV aneurysm with thrombus, prosthetic heart valve, myxoma, paradoxical embolus from patent foramen ovale, peripheral arterial or aortic atherosclerotic plaque embolism

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111
Q

Where is the most common site of peripheral obstruction from emboli?

A

Common femoral artery

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112
Q

When do you do a fasciotomy after an embolectomy?

A

If ischemia is greater than 4 to 6 hours. Aorto iliac emboli can be treated with bilateral femoral artery cutdowns and bilateral embolectomies

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113
Q

What are the indications for nephrectomy with renal hypertension?

A

Atrophic kidney less than 6 cm and minimal collaterals with persistently increased renin levels

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114
Q

Acute on chronic arterial thrombosis caused by arrhythmia? Hx? Tx?

A
  • Usually do not have arrhythmias.
  • Have a history of claudication and chronic ischemia.
  • Limb is threatened: give heparin, OR thrombectomy
  • Limb not threatened: angiography for thrombolytics.
  • Thrombosis of PTFE graft: thrombolytics and anticoag.
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115
Q

Where is the right renal artery run in relationship to the IVC?

A

Posterior to the IVC

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116
Q

What percentage of patients have accessory renal arteries?

A

25%

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117
Q

Where do most renal emboli come from?

A

The heart

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118
Q

In what patients does renal atherosclerosis occur, and in what part of the artery

A

Men, proximal one third of artery, left side. Treat with PTA and stent.

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119
Q

Fibromuscular dysplasia - what patients, what part of artery?

A

Women, right side, distal one third of artery. Treat with PTA.

120
Q

So what symptoms are suggestive of renovascular hypertension?

A

Bruits, diastolic blood pressure greater than 115, worsening hypertension, rapid onset after age 50, hypertension resistant to drug therapy

121
Q

What is the most common site of upper extremity stenosis?

A

Subclavian. Proximal lesions usually asymptomatic secondary to collaterals. Treat with stent; can also perform common carotid to subclavian bypass

122
Q

What is subclavian steal syndrome?

A
  • Proximal subclavian artery stenosis resulting in reversal of flow through ipsilateral vertebral artery into subclavian.
  • OR with limb or neurologic symptoms.
  • Tx: carotid to subclavian bypass or PTA.
123
Q

Where is the normal subclavian vein?

A

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

124
Q

Where is the normal brachial plexus and subclavian artery?

A

Pass over the first rib posterior to the anterior scalene muscle, and anterior to the middle scalene muscle.

125
Q

What is Adson’s test?

A

Decreased radial pulse with head turned ipsilateral side. Subclavian artery compression.

126
Q

What is tinsel’s test?

A

Tapping reproduces symptoms of thoracic outlet syndrome

127
Q

In thoracic outlet syndrome what is more common neurologic or vascular involvement?

A
  • Neurologic is more common.
  • The number one abnormality is the cervical rib.
  • The number one cause of pain is brachioplexus irritation
128
Q

With thoracic outlet syndrome what are the neurologic symptoms? Distribution? Dx? Tx?

A
  • Increased back and neck symptoms.
  • Ulnar nerve distribution. C8-T1 is common.
  • Can get triceps weakness and atrophy, weakness of intrinsic muscles of the hand, weak wrist flexion.
  • Dx: clinical for neuro-TOS
  • Tx: nTOS tx w/ PT and wt loss, decompression if no improvement
129
Q

What is Paget-von-Schrotter disease?

A
  • venous TOS 2/2 chronic injury to SCV at costoclav space
  • Psx: Effort thrombosis of SCV in athlete, palpable pulses
  • Dx: US 1st, XR for bones, CT/MR to define outlet obsx
    • venography gold standard, not often used
    • pulses r/o arterial dz, neuro exam to r/o plexus dz
  • Tx: depends on sx severity and timing
    • mild/intermittent sx - heparin anticoag only
    • severe sx - anticoag, thrombolysis, decompx
    • late psx (2 wks) - anticoag, decompression
    • three months of anticoagulation
130
Q

What is mortality from mesenteric ischemia?

A

50-70%

131
Q

What are findings of mesenteric ischemia on CT?

A

bowel thickening, intramural gas, portal venous gas, vascular occlusion

132
Q

What are causes of visceral ischemia?

A
  • Acute embolic occlusion 50%
  • Thrombotic occlusion 25%
  • Low-flow state 15%
  • Venous thrombosis 5%
133
Q

Superior mesenteric embolism occurs in what area of SMA? Psx? Dx? Mgmt?

A
  • Past origin of SMA. Pain out of proportion, sudden onset hematochezia, peritoneal signs late finding.
  • Dx: CTA shows oval occlusion surrounded by contrast in non-calcified artery, distal to branch point
  • First: NPO, NGT, IVF, abx, anticoag, PPI, O2
  • Tx: rule out peritonitis
    • arteriogram w/ thrombolysis
    • if fails: open embolectomy, may need bypass
      • if resect infarcted bowel, do second look
134
Q

What are signs of mesenteric artery thrombosis?

A
  • Sx: food fear, wt loss
  • Dx: CTA - thrombus on heavily calcified SMA ostia
  • First: NPO, NGT, IVF, anticoag, abx, PPI, O2
  • Tx: diffx thrombus vs embolus, r/o peritonitis
    1. No peritonitis: arteriography w/ thrombolysis
    2. PTA/stent (usually only for thrombus)
    3. if above fails: open
      • no dead bowel: thrombectomy vs bypass
      • dead bowel: resect, 2nd look
135
Q

What are signs of mesenteric vein thrombosis? Dx? Tx?

A
  • Short segments of intestine involved, bloody diarrhea, crampy abdominal pain. Vague abdominal discomfort present for a week or more, mild leukocytosis, and mild abdominal distention may be the only signs early in the course of the disease. Can occur as primary disease process.
  • Dx: CT angio, hypercoag testing
  • Tx: heparin, possible thrombolytics, abx, 6 mo anticoag
    • OR and bowel resection if peritonitis
136
Q

Non-occlusive mesenteric ischemia happens when? Dx? Tx? Prognosis?

A
  • Spasm, MI, sepsis, CV dz, cocaine, dialysis, hypovolemia, Digoxin. Watershed areas. Abd pain.
  • Dx: CTA w/o oral
  • Tx: IVF, NGT, abx, correct acidosis, avoid pressors
    • resect bowel if peritonitis - delay anastomosis
  • Prognosis: 70-90% mortality
137
Q

What is Median arcuate ligament syndrome?

A

Celiac compression. Bruit near epigastrium, chronic pain, weight loss, diarrhea. Tx: transect median arcuate ligament, may need arterial reconstruction

138
Q

Chronic mesenteric angina sx? Dx? Tx?

A
  • Sx: food fear, dull/crampy 30 postprandial, worse w/ fatty meals, subsides; progressive; weight loss
  • Dx: often delayed, r/o cancer, nutritional status
    • CT angio: calcifications, stenosis in 2/3 mesenteric vessels (or hx of surgery that disrupts 1), collaterals
  • Tx: stop smoking, secondary prevx, ASA
    • acute on chronic - anticoag
    • PTA, bypass, endarterectomy
139
Q

What is the most common complication of aneurysms above inguinal ligament?

A

Rupture

140
Q

What is the most common complication of aneurysms below inguinal ligament?

A

thrombosis and emboli

141
Q

What do you do with splanchnic aneurysms?

A
  • splenic and hepatic most common, often incidental
  • determine anatomy - if there are collaterals
    • usually CTA, but US good for liver (intrahepatic)
  • Pseudoaneurysms: repair/graft/stent, occlude if unable
  • Aneurysms: 2cm size, 0.5cm/year growth, pregnant woman, woman in childbearing years, during OLT
  • emergent: open exploration, ligation w/o reconstruction
  • elective: endovasc - if collaterals, can embolize proximal and distal; if no collaterals, stent
142
Q

What do you do with splenic artery aneurysms?

A
  • Most common visceral aneurysm
  • More common in women
  • Psx: 25% w/ abdominal pain and contained rupture
    • blood will be in lesser sac, chance to fix before it becomes intraperitoneal (48 hrs)
  • Rupture tx: ligation/embo proximal and distal to aneurysm
  • Elective tx: repair if symptomatic, pregnant, women of childbearing age.
143
Q

What dilatation of visceral arteries is considered aneurysmal?

A

>2cm

144
Q

If unable to repair, what can you do with splenic and common hepatic aneurysms?

A

can exclude - have good collaterals

145
Q

What are the surgical indications for iliac a aneurysms?

A
  • symptomatic, thrombosis, emboli, compression, >3.0cm - endovascular repair when possible, open if internal iliac must be preserved
  • mycotic - bypass with exclusion
146
Q

What are surgical indications for femoral a aneurysm?

A
  • symptomatic, >3cm
  • usually done open w/ reconstruction
  • endovascular reserved for emergency or those who cannot tolerate open surgery
147
Q

What are the surgical indications for popliteal aneurysms?

A
  • Exclusion and bypass if mycotic, >2cm, sx
  • Endovascular if unable to go to OR, not infected
  • 1/2 bilateral, 1/2 have another aneurysm elsewhere
  • Thrombosis and emboli most common psx - anticoagulation, thrombolysis, then repair
  • Medial approach if proximal disease, posterior approach if focal to popliteal fossa
  • Follow with US
148
Q

What do you do with a femoral pseudoaneurysm?

A

If after percutaneous intervention, need US guided compression with thrombin injection. May need surgical repair if this fails-collection of blood in continuity with the arterial system but unenclosed by all 3 layers of the wall

149
Q

What are the surgical indications for renal A aneurysms?

A

symptomatic, expansion, >2 cm, women who want to get pregnant; reconstruction with vein patch; nephrectomy with rupture

150
Q

Fibromuscular dysplasia?

A
  • Young women, HTN if involves renals. Renal most commonly involved vessel (right), carotid next, iliac next
  • String of beads on imaging
  • Medial fibrodysplasia most common variant
  • PTA if possible, bypass (saphenous vein graft)
151
Q

What is Buerger’s disease?

A

Pt: young men, smokers. Sx: severe rest pain, gangrene of digits. Findings: normal arterial tree proximal to popliteal and brachial, corkscrew collateral on angiogram w/ severe distal disease. Tx: stop smoking or amputate.

152
Q

What diseases cause cystic medial necrosis?

A

Marfan’s, type I collagen Ehlers-danlos. Tendency for arterial rupture. Can’t do angiogram - risk of laceration of vessel.

153
Q

What is temporal arteritis?

A
  • Giant cell arteritis - granulomatous disease, inflammation of large vessels, long segments of smooth stenosis alternating with segments of larger diameter.
  • Psx: headache, transient monocular visual loss, jaw claudication, fever, arthralgia, myalgia, anorexia.
  • Dx: temporal artery biopsy (don’t delay tx)
  • Tx: Steroids, no endarterectomy; prevent blindness.
154
Q

What is takayasu’s?

A
  • same path, sx, and tx of temporal a
  • PTA and bypass can be used
  • aortic regurg may require surgical therapy
155
Q

What is polyarteritis nodosum?

A
  • Get aneurysms that thrombose or rupture. Renals most common.
  • Dx: biopsy
  • Tx: steroids
156
Q

What is Kawasaki’s disease?

A

Affects children - get dilated coronaries and brachiocephalic vessels. Die from arrhythmias. Tx: steroids, possible CABG

157
Q

What is hypersensitivity angiitis (cutaneous small vessel vasculitis)?

A
  • Secondary to drug/tumor antigens.
  • Psx: rash, fever, palpable purupura and nonblanching petechiae, rarely end-organ dysfunction
  • Dx: biopsy skin lesions
  • Tx: Ca+ channel blockers, pentoxifylline
158
Q

What happens with radiation arteritis?

A

Sloughing and thrombosis, early fibrosis, scar, stenosis in 1-10 years. Advanced atherosclerosis 3-30 years

159
Q

Raynaud’s disease?

A

Pt: young women, pallor, cyanosis, rubor. Tx: Ca2+ blockers, warmth

160
Q

Where is the great saphenous vein?

A

joins femoral vein near groin - runs medially

161
Q

Where is the lesser saphenous vein?

A

joins popliteal in lower leg - runs lateral at first

162
Q

Can you ligate left renal vein?

A

yes- gonadal/adrenal vein collaterals

163
Q

What is the most common cause of failure of AV grafts?

A

venous obstruction secondary to intimal hyperplasia

164
Q

What is a Cimino graft?

A

radial artery to cephalic vein- wait 6 weeks

165
Q

How long before an interposition graft can be used?

A

6 weeks to allow fibrous scar to form

166
Q

How do you get an acquired AV fistula

A

Trauma. Can get peripheral insufficiency, CHF, aneurysm, limb length problems. Tx: repair with lateral venous suture, may need bypass of arterial side.

167
Q

Varicose veins: risks, psx, dx, mgmt

A
  • risks: smoking, obesity, low activity
  • psx: visibly dilated lower extremity veins; aching, swelling, heaviness
  • dx: venous duplex - superficial or deep
  • tx: stockings, elevation, exercise
    • cont sx and documented saphenous reflux:
      • 1) laser or RF ablation for saphenous
      • 2) sclerotherapy for larger varicose, laser for smaller
168
Q

Venous ulcers: risks, psx, dx, mgmt

A
  • Risks: valve incompetence; obesity
  • Sx: pain and heaviness worsening through day
  • Dx: US to determine reflux (after 6 mo med mgmt)
  • Tx: elevation, exercise, compression
    • debride if infected (GNB)
    • unna boot cures 90%
    • ASA
    • if saphenous reflux, do vein ablation
    • after 12 months, consider grafts
169
Q

Venous insufficiency symptoms?

A

aching, swelling, night cramps, brawny edema; ulceration above and posterior to malleoli; edema secondary to incompetent perforators

170
Q

How do you perform a trendelenburg test?

A

Elevate leg, occlude greater saphenofemoral vein junction, lower leg, rapid filling of greater saphenous vein suggests incompetent perforators. If first part did not fill, release pressure on saphenofemoral jxn- rapid filling suggests incompetent valves in greater saphenous.

171
Q

What is superficial thrombophlebitis?

A
  • Nonbacterial inflammation
  • Tx: NSAIDS, warm packs, ambulation; no anticoagulation needed unless increased risk for DVT
172
Q

What is suppurative thrombophlebitis?

A
  • Psx: usually in upper extremity after line placement or drug abuse. Venous thrombi can also be infected 2/2 bacteremia or contiguous spread.
  • S. aureus if peripheral, or 2/2 flora of contiguous structure
  • Sx and dx: fever, increased WBC; painful, red, palpable cord-like structure w/ purulent drainage
  • Tx: remove source (CVL), abx (vanc/ceftx x2-4 wks), anticoag if thrombus extension or deep, resect vein if no response and superficial
173
Q

What is migrating thrombophlebitis a sign of?

A

pancreatic CA

174
Q

what is Mondor’s Disease?

A

self limiting thrombophlebitis of the breast

175
Q

How do SCD’s work?

A

help prevent blood clots by decreasing venous stasis, increasing AT-III, tPA, increased fibrinolysis

176
Q

Where is DVT most common?

A

calf

177
Q

what is Virchow’s triad?

A

stasis, hypercoagulability, vessel wall injury

178
Q

How much swelling do you get with calf DVT?

A

minimal swelling

179
Q

Where is the swelling with femoral DVT?

A

ankle and calf swelling

180
Q

What swelling do you get with iliofemoral DVT?

A

severe leg swelling

181
Q

What is phlegmasia alba dolens?

A

tenderness, pallor, edema with DVT

182
Q

What is phelgmasia cerulea dolens

A

tenderness, cyanosis, massive edema

183
Q

From where can you get a PE with filter in place?

A

ovarian veins, inferior vena cava, upper extremity

184
Q

What do you do with venous thrombosis with a central line?

A

pull out if not needed, try to tx with heparin or TPA down line

185
Q

What lab findings do you see with PE?

A
  • Decreased paO2
  • Decreased PaCO2
  • Increased RR
  • Alkalosis
  • Most arise from above knee
  • If in shock - IR for pulmonary artery thrombectomy
186
Q

Do lymphatics have a basement membrane?

A

no

187
Q

Where are lymphatics not found?

A

bone, muscle, tendon, cartilage, brain, cornea

188
Q

When does lymphedema occur? Dx?

A
  • Obstruction, too few in number, nonfunctional woody edema secondary to fibrous tissue in subcutaneous tissue.
  • Cellulitis and lymphangitis secondary to minor trauma-strep most common infection
  • Dx: lymphoscintigraphy confirms
    • MRI/CT can be used to determine if there is a mass causing outflow obsx
189
Q

What side is congenital lymphedema most common?

A

Left

190
Q

What do you see with lymphangiosarcoma?

A

raised blue/red coloring; early mets to lung

191
Q

What is stewart treves syndrome?

A

lymphangiosarcoma associated with breast axillary dissection

192
Q

what is lymphangiectasia?

A

Dilation of preexisting lymphatic channels. Dx with lymphangiography. Tx with resection

193
Q

When do you get lymphocele?

A

after surgery; rule out infectious source first

194
Q

How do you identify lymphatic channels going to a lymphocele?

A

Inject isosulfan blue into foot to id channels. Tx: resect lymphocele and ligate supplying channel

195
Q

What pathology is described as an elevation of interstitial pressure in a closed fascial space resulting in microvascular compromise and cellular hypoxia?

A

compartment syndrome

196
Q

Once compartment pressure increases past a threshold, arterial perfusion diminishes causing ischemic damage leading to release of abnormal metabolic products. What two organ systems are most readily compromised by this?

A
  • cardiac - arrhythmia
  • renal - increased Cr
  • K, Ca, and myoglobin released from sarcoplasm
197
Q

What is the most common cause of compartment syndrome?

A

fracture (can occur in both open and closed)

198
Q

What compartment is most commonly affected after fracture?

A

anterior leg - fracture of tibia; hemorrhage, hematoma, edema all increase pressure

199
Q

Isolated soft tissue injury causes compartment syndrome where most often?

A

deep posterior compartment

200
Q

These non-trauma injuries should put what pathology on your differential?

reperfusion after ischemia, iatrogenic IVF extrav, electrical burns, DVT causing outflow obstruction, improper bandaging, improper positioning during surgery

A

compartment syndrome

201
Q

How do you diagnose compartment syndrome?

A
  • Clinically - known insult, pain out of proportion refractory to pain medication, tense/hard/woody compartment, edema, sensory/motor dysfunction, pain with passive stretching. Arterial pulse may still be palpable.
  • If equivocal or in pt who is not awake/alert/cooperative, check compartment P: delta P (from diastolic) <30. Absolute P >30 (high false positive rate).
  • If clinical or compartment P negative, do serial exams.
202
Q

How do you manage compartment syndrome?

A
  • start moving to the OR
  • in the meantime, remove all external compression, place limb at level of the heart, supplement O2, IVF as needed, address hyperkalemia
  • time to fasciotomy is the most important factor - within 4 hours is target (can expect full recovery), irreversible injury is expected after 12 hrs
203
Q

What are the essential components to fascial decompression?

A
  1. long overlying skin incision
  2. incise fascia along entire length
  3. local wound care of open incisions
  4. debride nonviable tissue - muscle bellies should appear viable; debride everything else; questionable areas can be left intact w/ intent to reassess within 24-48 hrs
  • postop: look for return of neuro fct - good fct prognosis
204
Q

What do you do with exposed ortho hardware of bypass grafts in fasciotomy for compartment syndrome?

A

cover with viable tissue

205
Q

What do you do if you suspect compartment syndrome?

A

Document findings and go to OR. The M/M from a missed fasciotomy is greater and more indefensible than an attempt to save a life/limb.

206
Q

In amputation for compartment syndrome causing necrosis in lower leg, how do you know if a BKA can be done?

A

one gastroc is viable; will likely need AKA if both gastrocs are dead

207
Q

What are the compartments of the lower leg and their associated nerves?

A
  1. anterior - deep peroneal nerve
  2. lateral - superficial peroneal nerve
  3. superficial posterior - sural nerve
  4. deep posterior - posterior tibial nerve
208
Q

Describe the two incisions used in the most common leg fasciotomy technique

A
  • lateral aspect of the leg over the interval between the anterior and lateral compartments (halfway between the crest of the tibia and fibula) from the head of the fibula to just above the lateral malleolus; incisions of fascia should be just anterior and posterior to the intermuscular septum
  • medial aspect of the leg along the posterior edge of the tibia (avoid saphenous); incise the fascia over the gastrocs to open the superficial posterior, incise the insertion of the soleus from the tibia to open the deep posterior
209
Q

What are often seen presentations of buttock compartment syndrome?

A

crush injuries or comatose patients who don’t get turned

210
Q

What is a fairly reliable physical exam finding to determine if there is thigh compartment syndrome?

A
  • pain with passive stretch
  • often seen with patients who have femur fractures or arterial injuries in the thigh
211
Q

Describe the relevant points of the thigh compartments

A
  1. anterior - femoral vessels and nerve, lateral cutaneous n
  2. medial - no major bundles, usually doesn’t need decompx
  3. posterior - sciatic nerve
212
Q

How do you decompress the thigh in compartment syndrome?

A
  • full-length lateral thing incision from the intertrochanteric line down to the lateral femoral epicondyle
  • anterior compartment - open the underlying fascia
  • posterior compartment - retract the vastus lateralis medially, open the lateral intermuscular septum
  • medial compartment - not usually opened, but can be decompressed with a medial incision like one used to expose SFA
213
Q

What are the compartments in the forearm?

A
214
Q

What nerve is most commonly impaired in forearm compartment syndrome?

A

median nerve - deeper, more vulnerable course than the ulnar nerve

215
Q

When should you suspect forearm compartment syndrome in children?

A

suspect forearm compartment syndrome in children following supracondylar fx of the humerus - can lead to ischemic contracture known as Volkmann contracture

216
Q

What incisions are used to decompress the forearm in compartment syndrome?

A
217
Q

Describe the compartments in the upper arm

A
  • anterior - radial n
  • posterior
  • both compartments can be decompressed through a lateral incision at the border of the biceps
218
Q

What neurologic finding is suggestive of compartment syndrome of the foot?

A
  • loss of two-point discrimination
  • long-term nerve loss leads to decreased proprioception and sensation which can cause ulcers
  • other sequelae include lesser toe deformity, cavus foot, ischemic contracture (quadratus plantae) causing a toe flexion deformity
219
Q

How many compartments are in the hand? What do you do if one of them is elevated?

A
  • four compartments
  • all should be measured individually if clinical diagnosis is unclear
  • if any are elevated, all compartments should be released along with the carpal tunnel
220
Q

Describe postop care in compartment syndrome

A
  • support for rhabdo, myoglobinuria, kidney damage
  • “shoelace” closure at time of fasciotomy with wound vac applied leads to higher rate of primary closure (as opposed to skin graft)
  • consider skin graft if closure cannot be achieved at 48 hrs
221
Q

Define intra-abdominal hypertension and abdominal compartment syndrome

A
  • IAH - sustained P > 12 mmHg (laparoscopic pressure)
  • ACS - sustained P >20 + organ dysfunction
222
Q

How do you manage abdominal compartment syndrome and intra-abdominal hypertension?

A
  1. ACS - OR for laparotomy
  2. IAH - sedate patient, loosen closure if possibe, consider diuresis or paracentesis
223
Q

What are the physiologic pulmonary effects of intra-abdominal hypertension?

A
  • decreased lung volumes - FRC and TV
  • intubated patients - increase peak inspiratory pressures, plateau pressures, and mean airway pressures
224
Q

Understand the effects of IAH on other organ systems

A
225
Q

Describe how to measure intra-abdominal pressure

A
  • supine position
  • sedated to relax abdominal muscles
  • time with end-expiration
  • instill 25 ml of sterile saline and measure P
  • continue q4h until suspicion decreases
  • avoid excessive fluids, sedate well, NGT decompression
226
Q

Is aspirin or clopidogrel more effective at reducing the incidence of primary endpoints of atherosclerotic disease (MI, stroke, death from other CV causes)?

Are there other increased risks when comparing the two?

A

Clopidogrel - this is especially true for the PAD population (as opposed to stroke and MI).

Clopidogrel increases risk of diarrhea, rash, and pruritis, but decreased risk of UGIB.

227
Q

What inflammatory marker is independently associated with the development of PAD?

A

CRP. In patients with established PAD, CRP is predictive of future CV events. These patients may benefit from statin use despite normal lipid levels.

228
Q

How do you manage claudication?

A
  • Exclude acute dz, confirm w/ ABI.
  • Prevention: control WT, DM, smoking, lipids, HTN. ASA or clopidogrel. Exercise.
  • If failing, add cilostazol.
  • If still failing, locate dz - CTA or MRA.
    • aortoiliac - angio/stent
    • fempop - is dz is limiting and dz length?
      • short/poor OR candidate - angio/stent
      • long - bypass
    • tibial - exercise
229
Q

How do you manage small, asymptomatic AAA?

A
  • no smoking - #1 modifiable factor for growth/rupture
  • start statin and ASA or clopidogrel
  • follow up q6-12mo w/ US or CT to look for growth
    • growth 0.5cm/6mo or 1cm/yr - EVAR
    • other aneurysms or PAD intervention - EVAR
    • woman w/ 5cm or man w/ 5.5cm - EVAR
    • severe CV dz w/ <2yr life - no repair
230
Q

Postop neurosurgery, when can VTE ppx be initiated?

A

48-72 hrs

231
Q

In thrombocytopenic patients requiring VTE ppx, what are the safe and unsafe platelet levels?

A
  • safe >50K
  • not used <25K
232
Q

When is heparin preferred to LMWH in VTE ppx?

A

CrCl <20-30 ml/min

233
Q

In pt w/ HIT, what medication is preferred for VTE ppx?

A

Fondaparinux

  • HIT complicates anticoagulation in 5% of cases.
  • Heparin PF4-AB complex binds PLT -> activation + low PLT.
  • B/w 5-10 days after exposure; PLTs drop by half, but >20K.
  • Sx: V or A thrombosis, skin necrosis, adrenal hemorrhage
  • Mgmt: 4T risk stratification
    • low: do not confirm, w/u other causes, observe
    • high: ELISA AB test; DC heparin/LMWH, start direct thrombin inhibitor (3 mo if thrombus).
234
Q

When can VTE ppx be stopped in a hospital patient?

A

When the pt is fully ambulatory. Extended ppx can be recommended in major abdominal surgery for cancer.

235
Q

What is the workup for a patient with suspected DVT?

A
  • determine pretest probability: surgery pt, edema, single swollen leg, swelling >3cm compared to other leg, local tenderness, cancer, bedridden, nonvaricose veins, no alternative diagnoses
  • for high PTP: do US w/ doppler
  • for low or med (0-2 risk facters): do D-dimer
236
Q

How do you manage a patient with high probability of PE who is unstable?

A
  • ABCs
  • able to resuscitate - immediate anticoagulation and CTPA
  • unable to resuscitate - bedside echo and US w/ duplex of lower extremities
    • echo shows PE evidence, thrombolysis
    • US shows DVT, start anticoagulation
237
Q

In a patient with PE who is unstable or who is stable with severe clinical symptoms (rare), what are the treatment options?

A
  • thrombolysis first line w/ anticoag postop
  • if thrombolysis is contraindicated, do surgical or catheter embolectomy
  • if thrombolysis fails to improve symptoms, do surgical or catheter embolectomy
238
Q

How do you manage a patient w/ PE and anticoagulation contraindication?

A

IVC filter

239
Q

What do you do with a stable patient with low to moderate suspected PE where diagnostic evaluation is going to take a long time? (all the CT scanners are broken)

A
  • start anticoagulation
  • await diagnostic evaluation
  • stop anticoagulation if ruled out
240
Q

For pregnant women with DVT, what is the medication of choice?

A

LWMH

241
Q

For patients with massive iliofemoral DVT or phelgmasia cerulea dolens w/ sx <14 days, what is the suggested treatment?

A

thrombolysis (systemic or catheter-directed) rather than anticoagulation alone

242
Q

How long should anticoagulation be continued for most patients with DVT?

A

3 months

243
Q

What patients benefit from indefinite anticoagulation after VTE?

A
  • unprovoked proximal DVT or PE
  • those with induced risk factors lasting longer than 3 months should have anticoagulation continued until risk resolves
  • INR target is 2-3
244
Q

In patients with suspected carotid stenosis, what is the workup?

A
  • carotid duplex ultrasound
  • >50% stenosis - MRA
    • findings not agreeing - CTA
  • <50% stenosis - annual exams
245
Q

When would angiography be performed for carotid disease?

A
  • gold standard, but rarely required
  • contraindication to MRI study and dye
  • poor quality of noninvasive studies
  • continued discordance of noninvasive studies
246
Q

When should carotid artery stenosis be treated with a stent?

A
  • surgical indication: 80% stenosis in asx or 70% with sx, stenosis <99%, life expectancy >5 yrs, <6% stroke/death risk at OR center
  • CAS: not surgically accessible, radiation-induced stenosis, clinically significant cardiac/pulmonary/other dz making CEA risky
247
Q

What is the management perioperatively for CEA?

A
  • before OR, need to start ASA and statin
  • abx ppx
  • general or local anesthesia
  • anticoagulate before clamping
  • reverse heparin w/ protamine at completion
  • always use a patch for closure
  • monitor neuro status and BP postop
248
Q

In bilateral carotid disease with surgical indication, how do you develop a plan?

A
  • symptomatic side first
  • if asx, and one side is more stenotic, do that one first
  • if asx, and stenosis is similar, do dominant side first
249
Q

You get consulted for a cold limb. How do you evaluate?

A
  • Likely won’t have palpable pulses
  • Handheld Doppler - arterial and venous
  • Neuro exam - strength and sensation
250
Q

How do you manage acute limb ischemia?

A
  • IVF and anticoagulation w/ heparin drip
  • Doppler pulse: viable - CTA, no intervention
  • No artery signal, no motor/some sensory def: marginal
    • CTA vs arteriogram, urgent revascularization
  • No artery signal, mild motor def: immediate
    • OR for imaging, emergent revascularization
  • No a/v signals, paralysis/anesthesia: nonviable - ampx
  • Once revascularized, find the source (echo, CT CAP to r/o cancer). Likely need ASA and statin
251
Q

In patients who received a drug-eluting stent, how long do they need to be on dual antiplatelet therapy before undergoing elective surgery?

A

6 months

ASA and clopidogrel

Hold clopidogrel for 5-7 days, continue ASA

252
Q

Indications for HD access

A

GFR 10-15 mL/min/1.73 m2 in a symptomatic patient or GFR < 5 mL/min/1.73 m2 in an asymptomatic patient.

Sx: AEIOU-Acidosis, Electrolyte abnormalities, Intoxication, Overload, Uremia

253
Q

Kidney Disease Outcome Quality Initiative recommends the following order of access preference for end-stage renal disease patients and patients expected to require hemodialysis:

A
  1. Autologous radiocephalic (forearm) arteriovenous fistula
  2. Autologous brachiocephalic arteriovenous fistula
  3. Transposed brachial-basilic arteriovenous fistula
  4. Upper arm brachial-cephalic prosthetic graft
254
Q

If radiocephalic or brachiocephalic arteriovenous fistulas cannot be established, the 2006 guidelines recommend the use of…

A

transposed brachial-basilic fistula over prosthetic arteriovenous grafts.

255
Q

If the basilic vein is used it should be transposed. Why?

A

close proximity of the median antebrachial cutaneous nerve

take care: basilic vein is thin-walled and thus is more prone to injury and devascularization during mobilization

256
Q

For an AV fistula to be considered successful, it must be usable. In general, a working fistula must have all the following characteristics:

A
  • Blood flow adequate to support dialysis: >600 mL/min
  • Diameter >0.6 cm in an accessible location for cannulation w/ discernible margins to allow for repetitive cannulation
  • Depth of approximately 0.6 cm (b/w 0.5–1.0 cm)
257
Q

For HD access through AVF, what are the vessel size requirements?

A
  • artery >2 mm, w/o significant inflow stenosis
  • vein >3 mm, w/o any outflow stenosis
  • small size up to the AC fossa means a brachiocephalic AVF is required
258
Q

After your AVF is created, you palpate pulsatile flow. What does this mean?

A

outflow obstruction

259
Q

When creating an AV fistula, what is the ideal vessel configuration?

A

End-of-vein to side-of-artery anastomosis (higher patency rates than side-to-side anastomosis)

260
Q

The definitive diagnostic test for vascular prosthetic graft infection is?

A

Operative exploration. Culture of the surrounding biofilm and graft excision is the only reliable method of identifying the causative bacteria and selecting the appropriate antibiotics.

CT can show signs. Exam is unreliable.

261
Q

Psx: Old, obese, smoking, diabetic male w/ a desk job who presents w/ weeks of lower extremity discomfort, swelling, aches that worsen through the day.

Exam shows dilated veins, edema, lipodermatosclerosis.

Dx?

A

Venous stasis

  • venous reflux 2/2 valvular incompetence
  • lipodermatosclerosis - fibrosing dermatitis of subcutaneous tissue
  • other assn: lymphedema, PVD, varicose veins, venous thrombosis
262
Q

Examples of contiguous infection causing suppurative thrombophlebitis include pelvic septic thrombophlebitis developing after ______ infections, ______ thrombophlebitis associated with severe pharyngitis and peritonsillar abscesses, and ______ stemming from appendicitis.

Compare to superficial vein thrombophlebitis.

A
  • obstetric
  • internal jugular
  • visceral thrombophlebitis

S aureus most common causative organism. GNB and coag neg staph possible w/ contiguous infection.

Contrast with superficial vein thrombophlebitis: more benign, less likely psx w/ fever or tenderness to palpation, no pus. Tx: remove IV, no need for cx or abx.

263
Q

Two months after placement of a brachial-cephalic fistula for dialysis, a 67-year-old female is complaining of pain in the hand below the fistula that worsens on dialysis. The dialysis unit does not feel that they can lower her flow rates as they are barely obtaining adequate dialysis. On exam, she has a cool hand with a radial signal detectable only by Doppler. Upon manual occlusion of the fistula, the hand becomes warm, and the radial pulse becomes palpable. Angiography shows the fistula to be patent without inflow or outflow obstruction.

What is happening? What do you do?

A

This patient has a symptomatic steal syndrome. By the second month after placement, the steal is unlikely to improve just by waiting. Angiography shows a patent fistula, so there is no role for angioplasty. Therefore, a Distal Revascularization and Interval Ligation (DRIL) procedure is the best choice. Banding of the fistula is unlikely to be helpful, especially if the flow rates are only adequate, any diminution would likely leave the fistula unusable, and ligation is premature. It would also be acceptable to pursue segmental pressures to better quantify the degree of steal.

264
Q

What lower leg artery is most likely to stay patent in a patient with chronic atherosclerotic disease?

A

peroneal artery

265
Q

What is a proximal DVT? What is the first step upon diagnosis w/ US? What is the role of thrombolysis/ectomy?

A
  • Thrombus located in the popliteal, femoral, or iliac veins.
  • Anticoagulant for all w/ proximal DVT, regardless of sx.
  • Thrombolysis/thrombectomy are reserved for patients w/ phlegmasia cerulea dolens (limb-threatening ischemia) or massive iliofemoral DVT (severe swelling) or for patients who fail therapeutic anticoagulation.
  • Lysis candidates should have sx <14 days (ie, fresh clot; organized clot will not undergo lysis), good function, low bleed risk.
266
Q

Asymptomatic aneurysms requiring early operation?

A
  • ascending thoracic - 5.5 cm or growth 1 cm/yr
  • descending thoracic - 5.5 cm or growth 1 cm/yr
  • abdominal - 5.5 cm or growth 1 cm/year
  • iliac - 3 cm or growth 1 cm/year
  • femoral - 3 cm or growth 0.5 cm/year
  • popliteal - 2 cm
267
Q

How do you perform ABI?

A
  • Need appropriately sized manual BP and Doppler.
  • Pt supine and allowed to rest before the exam.
  • Place BP cuff above ankle. Doppler the DP and PT pulse. Inflate the cuff until signal is obliterated. Release the cuff, and record P when signal returns (DP vs PT). Keep the highest one.
  • Repeat for both legs (DP and PT signals) and both arms.
  • ABI = higher ankle P (DP vs PT)/highest arm P (L vs R).
  • Normal ABI is 0.9 to 1.2.
  • Claudication is usually from 0.5 to 0.9.
  • Rest pain or tissue loss usually have ABI less than 0.5.
268
Q

Following a midfoot amputation for multiple digital infections, a patient with diabetes is assessed for healing potential. An ankle-brachial index is performed, and this demonstrates a value of 0.3 in the affected foot. What would be the next step to improve the wound healing potential in this patient?

A

Pt has severe PAD. With this degree of disease, the wound healing potential is poor. This patient will require some type of intervention to improve the circulation in the foot. An angiogram would allow for a possible intervention or would provide preoperative planning for a larger vascular reconstruction. Anticoagulation alone will not increase the perfusion to the patient’s leg. Offloading of the wound is an important aspect of wound healing; however, the patient must have adequate circulation in order for the wound to heal.

269
Q

A 49-year-old woman with diabetes presents with a large, erythematous right first toe with expressible purulence. She has no palpable pulses, and pedal Doppler signals are faint. Her ankle pressures are not obtainable due to noncompressible vessels. What is the most appropriate management?

A

The first treatment priority is surgical drainage in the form of an open toe amputation. Failure to address her foot abscess will likely result in limb loss regardless of her arterial perfusion. After her acute infection resolves, she will require some form of revascularization to allow her amputation to heal.

270
Q

Discuss femoral artery aneurysm after aortofemoral bypass.

A
  • Femoral anastomotic aneurysm (FAA) is a rare complication after aortofemoral reconstruction for occlusive or aneurysmal disease. FAAs may develop among 6%.
  • Development of an FAA after autogenous tissue reconstruction such as femoropopliteal bypass is very rare.
  • Host-vessel degeneration is the most commonly cited etiology.
  • Because of the complications of progressive outflow occlusion from embolization of FAA laminated thrombus, even asymptomatic FAAs larger than 2 to 2.5 cm in diameter should be repaired. All symptomatic FAAs require repair, provided the patients are acceptable operative risks. Interposition grafting from the old prosthesis to a suitable outflow vessel, often only the deep femoral artery, using a short segment of polytetrafluoroethylene graft material is the operative procedure of choice.
  • Minimal debridement and working from within the aneurysm sac itself minimizes postoperative neurovascular complications.
  • Excision is not required.
  • A small number of FAAs recur and should be managed like other FAAs with excellent results to be expected.
271
Q

Discuss graft failure after placement for arterial disease.

A
  • Early graft failure is defined as occurring within 30 days.
    • 2/2 a technical error: twists, kinks, incompletely lysed valves, use of poor quality vein or outflow target.
  • Intermediate graft failure occurs between 30 days to 2 years.
    • 2/2 intimal hyperplasia at anastomoses or old valves.
  • Late graft failures occur > 2years post-operatively a
    • 2/2 progressive atherosclerotic disease within inflow or outflow arteries.
  • Surveillance duplex: may help ID grafts at high risk of failure. Absolute velocities of less than 40cm/sec or greater than 300cm/s, or a 3x increase in velocity in one segment compared to the adjacent one suggest impending graft failure.
272
Q

Physical exam reveals a cold right leg with pallor and poor capillary refill from the mid-calf to the foot. There are no pedal pulses and only faint arterial monophasic Doppler signals. The right common femoral artery has a bounding, strong pulse. Based on the above physical exam, where did the embolus lodge?

A

Below-knee popliteal artery

273
Q

How do you access the supraceliac aorta?

A

Accessing the supraceliac aorta requires mobilizing the left lobe of the liver and dividing the triangular ligament. In addition, the esophagus must be identified and reflected to the patient’s left. This is aided by placement of a nasogastric tube.

274
Q

Transient neurologic adverse effects such as visual disturbance, migraine-like headache, or confusional state may occur with sclerotherapy (done for venous disease), and are more frequent in patients with…

​

A

patent foramen ovale

275
Q

In a patient with varicose veins, a medial lower extremity ulcer is associated with reflux in what vein?

Lateral ulcer?

A

incompetent great saphenous vein

Incompetent small saphenous vein

276
Q

What are some indications for PTA?

A
  • RAS w/ HTN or deteriorating renal function
  • medial FMD lesions
  • non-ostial renal artery lesions (ostial don’t respond)
  • common iliac, short/focal vessel disease
    • open bypass for EIA/femoral/popliteal dz
    • add stent: plaques, dissection, residual stenosis, recurrent stenosis
  • follow with aspirin
277
Q

Deep venous thrombosis resulting from upper extremity central venous lines should be treated how?

A

catheter removal, heparin therapy, and long-term oral anticoagulants

The process is not self-limiting. Catheter removal and early systemic heparin followed by warfarin (Coumadin) therapy for three to six months is the preferred current therapy to prevent PE and their sequelae.

278
Q

Using an ultrasound on the groin, how do you find the GSV, CFA, and CFV?

A

Both the great saphenous vein and the common femoral vein lie medial to the common femoral artery. Using the “Mickey Mouse” sign, the great saphenous vein appears more superficial and represents Mickey’s medial ear.

The common femoral artery lies laterally to the great saphenous and common femoral veins. The common femoral vein lies in between the common femoral artery and the great saphenous vein.

279
Q

After vascular reconstruction, how are patients surveilled?

A

Duplex US and physical exam q6mo x2 yrs.

280
Q

For an AVF that cannot be accessed but can be palpated, what is a good workup?

A
  • Start w/ Duplex US to look for anatomic etiology - failure of maturation due to an anatomic cause such as stricture, fistula may be too deep (obese) to cannulate with two needles.
  • Fistulagram would be useful as a follow-up study if an anatomic etiology found for percutaneous intervention.
  • Depending on findings, percutaneous (angioplasty) or surgical revision, or (adequate diameter) vein fistula superficialization/elevation can be done.
281
Q

A patient with a ruptured AAA is coming in. What do you need to have prepared?

A

Have at least three aortic excluding balloons available.

Establishing supraceliac aortic control is essential in keeping these patients alive - done endovascularly with an aortic excluder balloon such as Coda balloon inserted percutaneously through the contralateral groin that one plans to insert the main body graft.

Prior to induction of general anesthesia: prep the patient from nipple line to midthigh bilaterally.

282
Q

After placement of a right internal jugular central venous catheter in the ICU, the resident suspects that the catheter may have been placed in the carotid artery. What is the most appropriate next step in management?

A

The first step in management is confirmation of arterial access either by transducing the catheter or obtaining an arterial blood gas through the catheter.

283
Q

Budd-Chiari syndrome definition and causes?

A
  • hepatic venous outflow obstruction
  • m.c. causes in the West are myeloproliferative dz: PCV, and essential thrombocytosis
  • disorders of coagulation lending to thrombus formation also have been implicated in the condition such as protein C and S deficiency, factor V Leiden mutation, and antiphospholipid antibody
  • oral estrogen is also associated to this
284
Q

How can you differentiate lymphedema from obesity?

A

obesity is symmetric with less feet involvement

285
Q

What is the most common reason for lower extremity amputation?

A

diabetes complication

286
Q

What is the common vascular reason for amputation?

A

critical limb ischemia w/ failed revascularization

287
Q

What are the goals of amputation?

A
  • debride infected/necrotic tissue
  • leave the longest stump possible
288
Q

What method of amputation has been associated with a lower complication rate in septic patients?

A

guillotine amputation followed by revision, this is compared to a single-stage procedure

289
Q

What is the periop DVT rate in a patient requiring amputation?

A

11%

290
Q

Discuss the fibula and tibia level of amputation in a BKA.

A

Fibula has to be divided at a higher level.

Tibia should extend 10-12 cm past tuberosity. Fibula should be 1-2 cm more proximal (higher) than this. Tibia can be as short as 5 cm.

291
Q

How do you prevent neuroma?

A

Divide nerves high and ligate them

292
Q

Describe how the skin closure should be at the end of the case.

A

Tension-free

293
Q

What are common reasons for failure of amputation wounds?

A

Trauma, ischemia, fluid collections, and infection

294
Q

What % of BKA patients will require revision to AKA?

A

25%

295
Q

What is the difference in increased energy expenditure in a BKA vs AKA?

A

BKA: 10-40%

AKA: 50-70%

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