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Surgery Clerkship > Vascular Disease and Vascular Surgery > Flashcards

Vascular Disease and Vascular Surgery Flashcards

1
Q

Stages of an ulcer

A
  • Based upon depth
    • Stage 1: Nonblanching erythema (only into epidermis, not down to dermis)
    • Stage 2: Dermis exposed
    • Stage 3: Fascia exposed
    • Stage 4: Muscle/bone exposed
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2
Q

Pressure ulcers

A
  • Due to persistent compression of an area in those who are bedridden or wheelchair bound. May indicated neglect if patient is a nursing home resident.
  • Most common areas: Buttocks, heel/over the calcaneus
  • Dx: Clinical
  • Tx: q2h rolls, move around / oob if possible, air-mattresses
    • Necrotic tissue: debridement
    • If cellulitis: Abx
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3
Q

Diabetic ulcers

A
  • Path: Microvascular changes + neuropathy
    • Neuropathy must be present for this to be the diagnosis
  • Pres: Ulcers on heels and balls of feet that are NOT PAINFUL
  • Dx: Clinical
  • Tx: Control blood glucose, elevate legs
    • May need to amputate
  • Ppx: Diabetic foot exams, make sure patient as good shoes
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4
Q

Arterial insufficiency ulcers

A
  • Path: Peripheral arterial disease
  • Pres: Hairless legs, shiny-scaly skin, absent pulses, often in smoker, present in tips of toes
  • Dx: That of PAD – ankle brachial index, US w/ doppler, angiogram
  • Tx: Stent (small lesions above knee) or bypass graft (popliteal artery or any large length lesion)
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5
Q

Venous stasis ulcers

A
  • Path: Venous insufficiency
  • Pres: Edema will be present with some predisposing condition, stasis dermatitis (hyperpigmentation from hemosiderin deposition), induration, classically on medial maleolus
  • Dx: Clinical
  • Tx: Compression stockings, elevate legs, diuretics
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6
Q

Marjolin ulcer

A
  • Path: Squamous cell carcinoma
  • Pres: Sinus tract, ulcer that breaks and heals over and over, heaped up margins
  • Dx: Biopsy
  • Tx: Wide resection
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7
Q

Abdominal aortic aneurysm

A
  • Etiology: Atherosclerosis
  • Pres: >65 year old male, current or former smoker with an asymptomatic pulsatile mass
    • Men > 65 who have smoked get a one-time screening ultrasound
  • Dx: US is preferred. CT scan may incidentally diagnose AAA, but suspected AAA is diagnosed by ultrasound.
  • Tx is size dependent:
    • 3-4 cm: screen q2y
    • 4-5 cm: screen q1y
    • 5.0-5.4 cm: screen q6mo
    • >5.5 cm: Operate
    • Increase of >0.5 cm/6 mo, operate.
    • Operation is either endovascular repair or open surgery, both equally successful.
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8
Q

Emergent presentation of abdominal aortic aneurysm

A

Patient presents with tender pulsatile mass and back pain, with a smoking history.

The back pain is referred pain from the aorta, which is experiencing stretch from the pressure. Take to the ER emergently or their aorta will pop.

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9
Q

Aortic dissection

A
  • Etiology: Chronic untreated hypertension
  • Pres: Tearing chest pain that radiates to back, assymmetric blood pressures in arms, widened mediastinum
  • Risk factors: Marfan syndrome, syphilis of the aorta
  • Type A is ascending, Type B is descending
  • Dx: CT angiogram looking for false lumen. If they have renal failure, TEE or MRI are preferred.
  • Tx:
    • Type A: Operate now. Evaluate for need to replace aortic valve.
    • Type B: Treat medically w/ IV beta blockers.
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10
Q

Differentiating claudiation pain from spinal stenosis

A
  • Claudication: Of distal extremities, non-positional pain
  • Spinal stenosis: “Claudication” of buttocks, positional pain
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11
Q

Subtle physical exam findings of peripheral vascular disease

A
  • Shiny shins
  • Loss of hair
  • Decreased pulse
  • Lower temperature
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12
Q

Peripheral vascular disease

A
  • Risk factors: HTN, DM, Hyperlipidemia, smoking, female, pre-existing CAD
  • Dx: ABI
    • If above 1.4, vessel is calcified. Try TBI instead. (toe brachial)
    • 1.0 - 1.3 is normal
    • 0.9 - 1.0 is equivocal, f/u with exercise ABI
    • 0.8-0.9 is mild PVD
    • 0.4-0.8 is moderate PVD
    • <0.4 is severe PVD
      • If positive, f/u with US w/ doppler
      • If positive, f/u with CT angiogram
  • Tx:
    • Whether or not to pursue angioplasty and stenting (above knee or small) or bypass grafting (below knee or large) is based upon utility of restoring perfusion – if person is active, sure. If bed-bound, maybe try medical management instead.
    • Medical management: Same as CAD, but don’t use anticoagulants, just antiplatelets. Cilostazol or pentoxyphylline improve symptoms, but not outcomes, and both are contraindicated in CHF.
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13
Q

Acute limb ischemia

A
  • Etiology: Cholesterol embolism following catheterization, clot embolism in AFIB, thrombus in setting of PVD
  • Pres: 6 P’s:
    • Pulseless
    • Pale
    • Poikilothermia (cold)
    • Pain
    • Paresthesias
    • Paralysis
  • Dx: US w/ doppler. If positive, emergent angiogram to identify vessel and reperfuse.
  • Tx: Embolectomy or intra-arterial tPA.
  • Complications: Compartment syndrome. If develops, need to cut open to relieve pressure.
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14
Q

Signs of neuropathic origin in a diabetic ulcer

A
  • Decreased touch sensation, reflexes, vibration sense (Not done routinely)
  • Location often plantar surface
  • Foot becomes “claw foot”, more prominent metatarsal heads
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15
Q

To rule out osteomyelitis in an ulcer, you should. . .

A

. . . probe it.

If you hit bone, you should be suspecting osteomyelitis. If not, it is pretty unlikely.

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16
Q

Popliteal entrapment syndrome

A
  • Etiology:
    • Can be due to an excessively muscular calf compressing the artery
    • Can be due to embryologic/anatomic defect involving an excess band of muscle or tendon which can easily compress the vessel
  • Often presents with claudication
  • Dx: Angiogram at rest and with extension/flexion of involved muscles. May be normal at rest and occlude with local muscle contraction.
  • Tx: Resect obstructing tissue
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17
Q

Adventitial cystic disease

A
  • Pathognomonic “scimitar sign” on imaging
  • Condition in which a cyst forms in the adventitia of an artery and narrows or blocks blood flow
  • Often presents with claudication
  • Always on Ddx for popliteal entrapment syndrome
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18
Q

Characteristic imaging feature of IgA vasculitis (aka Berger’s disease)

A

Corkscrew collaterals

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19
Q

5 P’s of compartment syndrome

A
  • Pain
  • Parathesias
  • Paralysis
  • Pulselessness
  • Poikilothermia (cold)
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20
Q

Post-embolectomy or thrombectomy patients are at high risk for ___, which can mimic ___.

A

Post-embolectomy or thrombectomy patients are at high risk for ischemia-reperfusion induced compartment syndrome, which can mimic deep vein thrombosis.

Usually, compartment syndrome will develop much sooner than you would expect to take a repeat DVT to form – on the order of hours for compartment syndrome vs days for DVT.

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21
Q

Categories of PAD

A
  • Intermittent claudication
    • Mild PAD, noncalcified vessel ABI > 0.40
  • Critical limb ischemia
    • Ischemic rest pain lasting > 2 weeks
    • In noncalcified vessel, ABI < 0.40
    • In calcified vessel, symptoms + toe pressure < 30 mmHg
    • Skin changes
    • Dependent rubor, elevation pallor
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22
Q

Leriche syndrome

A
  • Triad of buttock / thigh claudication, impotence, and diminished femoral pulses
  • This indicates iliac artery occlusive disease in a male
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23
Q

Generally speaking, interventions for arterial occlusive disease tend to work better in ___ than in ___.

A

Generally speaking, interventions for arterial occlusive disease tend to work better in large arteries than in small arteries.

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24
Q

Approach to type A, B, C, and D vascular stenotic lesions

A

Type A: Endovascular repair is the clearly favorable approach

Type B: Good results using endovascular repair, but open may be performed if it is needed for another lesion in the same anatomic region

Type C: Better long-term results with open revascularization than endovascular, so open should be performed unless patient is a high risk candidate for open surgery.

Type D: Poor results with endovascular treatment, open revascularization is the clear choice.

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25
Q

Treatment for arterial thromboembolism to distal extremity (in the setting of afib)

A

Heparinization and embolectomy

Catheter directed thrombolysis is an option, but it is too slow. We need to save this person’s extremity, so we have to act quickly.

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26
Q

Distinguishing vascular and neurogenic claudication

A

Vascular is going to be consistent, and will typically not be relieved by positional changes (except in the case where this increases bloodflow)

Neurogenic may be inconsistent and often be relieved by positional changes

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27
Q

Criteria for AAA repair

A
  • Diameter > 5.5 cm in men OR > 5.0 cm in women
  • Growth of > 0.5 cm / 6 months
  • Symptomatic AAA (pain, distal embolic disease)
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28
Q

If an AAA does not meet criteria for repair, you. . . .

A

. . . monitor it

  • 2.6-2.9 cm: every 5 years
  • 3.0 to 3.4 cm: every 3 years
  • 3.5 to 4.4 cm: every year
  • 4.5 to 5.4 cm: every 6 months
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29
Q

Risk modification for control of AAA expansion

A
  • AAA expansion can be minimized by controlling:
    • Hyperlipidemia
    • Hypertension
    • CAD
30
Q

Inherited conditions associated with aneurysm development

A
  • Marfan syndrome (Fibrillin)
  • Ehlers-Danlos syndrome (Type V collagen)
  • Familial Thoracic Aneruysm and Dissection syndrome (aka TAAD syndrome)
31
Q

USPSTF AAA screening recommendations

A
  • Men age 65-75 who have ever smoked get a one time screening
  • Men age 65-75 who have never smoked but have other significant risk factors get a one time screening
    • Screening is never performed in women as their risk is substantially lower
32
Q

Endoleaks following EVAR

A

Persistence of bloodflow outside of the endocraft following EVAR (endovascular aneurysm repair).

Endoleaks are the most common reason for secondary intervention after EVAR.

33
Q

Types of endoleak

A
  • Type 1: Caused by inadequate sealing at the proximal or distal endograft attachment sites
  • Type 2: Caused by blood flow into the aneurysm sac from patent branch vessels
  • Type 3: Caused by a defect in the fabric of the endograft or leakage between separate graft components deployed
  • Type 4: Leaking between the interstices of the graft fabric
  • Type 5 (aka endotension): Aneurysm sac that remains pressuried without vissible endoleaks
34
Q

Best predictors of AAA rupture

A
  • Size
  • Symptoms
35
Q

Most AAAs are located. . .

A

. . . in the infrarenal aorta

36
Q

Monitoring following EVAR vs open repair

A
  • EVAR:
    • CT scans at 1 month and 12 months
      • Most endoleaks occur early
      • 20-30% risk of secondary intervention requirement at 6 years
  • Open:
    • CT scan every 5 years
37
Q

Anyone diagnosed with AAA should have an exam to. . .

A

. . . assess for aneurysmal disease at other locations

38
Q

AAAs are papable in the ___

Iliac aneurysms are palpable in the ___

A

AAAs are papable in the epigastrium

Iliac aneurysms are palpable in the infraumbilical region

39
Q

While the risk of AAA is higher in ___, the risk of rupture of an existing AAA is higher in ___.

A

While the risk of AAA is higher in men, the risk of rupture of an existing AAA is higher in women.

40
Q

Triad of mesenteric ischemia

A
  • Postprandial pain
  • Food fear
  • Unintentional weight loss
41
Q

Presentation of acute mesenteric ischemia

A

Initially, pain out of proportion to exam findings is characteristic.

However, at some point intestinal necrosis and peritonitis will set in, and then this will dominate the picture.

42
Q

Vascular blood supply of the mesenteric vessels

A
43
Q

SMA thrombosis vs SMA embolism

A
  • SMA embolism: In the setting of MI or atrial fibrillation. Sudden onset without any preceding symptoms of chronic mesenteric ischemia. Generally better prognosis than SMA thrombosis, since luminal involvement is incomplete.
  • SMA thrombosis: In the setting of chronic mesenteric ischemia, and so there will be a prior history of mesenteric angina. Generally worse prognosis than SMA embolism, since luminal involvement is often complete.
44
Q

Chronic mesenteric ischemia generally only becomes symptomatic after ___

A

Chronic mesenteric ischemia generally only becomes symptomatic after multiple vessels are involved

Since there is so much collateral bloodflow in the mesentery

45
Q

Nonocclusive mesenteric ischemia

A
  • Occurs in hosptalized patients with prolonged hypotension
    • Often in association with administration of vasopressors or other vasoconstrictive medications like digoxin and dopamine
  • Ischemic pattern produced does not follow typical anatomical boundaries, and are generally characterized by patchy necrosis
  • Tx involves support of cardiac output and blood flow to the intestines with resection of non-viable intestine as needed.
    • Systemic anticoagulation may be helpful to minimize extension of mesenteric thrombosis
46
Q

Median arcuate ligament syndrome

A
  • Uncommon form of mesenteric ischemia
  • Produced by extrinsic compression of the celiac artery by the median arcuate ligament
  • Treated by decompression involving division of the arcuate ligament in conjunction with endovascular stenting or surgical reconstruction of the celiac artery
47
Q

Watershed regions of the intestinal tract

A

The splenic flexure (between SMA and IMA distributions)

The mid-low rectum (between IMA and rectal artery distributions)

48
Q

A patient with chronic mesenteric ischemia almost always has ___

A

A patient with chronic mesenteric ischemia almost always has significant weight loss

If this is not present, it is unlikely to be chronic mesenteric ischemia/mesenteric thrombosis

49
Q

Chronic mesenteric ischemia is much more common in ___ than ___.

It is believed that this is due to ___.

A

Chronic mesenteric ischemia is much more common in women than men.

It is believed that this is due to different angulation of the SMA-aorta vertex between men and women

50
Q

Patient presents with TIA and is found to have bilateral carotid stenoses >80%. What are the next steps in management?

A
  • Risk factor control:
    • Place on DAPT
    • Place on statin
    • Smoking cessation
    • Blood pressure control
  • Source control:
    • Bilateral carotid endarterectomies within two weeks starting with the symptomatic carotid
51
Q

When do we intervene on patients with carotid stenosis

A
  • >50% with symptoms (TIA, stroke)
  • >60% without symptoms
52
Q

Amaurosis fugax

A
  • “fleeting darkness” in Greek
  • Temporary blindness caused by TIA
53
Q

Carotid artery stenting

A
  • Done percutaneously
  • Carries risk of intraoperational stroke – therefore usually done with cerebral protection devices downstream in the carotid
54
Q

CEA or medical management for carotid stenosis

A

CEA always carries a lower risk long-term, but the degree of risk reduction relative to medical management varies

55
Q

__% of patients with carotid bruits on exam have carotid stenosis > 30%

A

50% of patients with carotid bruits on exam have carotid stenosis > 30%

And even fewer have carotid stenosis that is more substantial.

In other words, just because a patient has a carotid bruit doesn’t mean that they have carotid stenosis or are at risk for strokes. Given this finding alone, the likelihood is still that they are not at risk, but they are worth screening with duplex ultrasoud.

56
Q

Role of CT angiography, MR angiography, and catheter-based angiography in carotid stenosis

A
  • CT angiography and MR angiography are not used for diagnosis, but may be useful in surgical planning. These are safe imaging modalities.
  • Catheter-based angiography is similarly used only for surgical planning, but also carries a risk of intraoperational stroke (~1-2%). As such, it should never be ordered for routine purposes – only when deemed absolutely necessary for surgical planning by the operative surgeon or interventional radiologist
57
Q

In patients who are very poor surgical candidates, specifically those with refractory CHF, ___ may be preferred for treatment of carotid stenosis

A

In patients who are very poor surgical candidates, specifically those with refractory CHF, medical management may be preferred for treatment of carotid stenosis

CEA just would not be an option.

58
Q

Complete internal carotid artery occlusion

A

These patients are not candidates for carotid endarterectomy

59
Q

Major perioperative complications of CEA

A
  • Stroke (obviously)
  • Myocardial Infarct (not so obvious. Unclear why this is the case, but empirically it does happen)
60
Q

Post-CABG atrial fibrillation

A

Common and self-limited

Resolution is typically within 24 hours, not requiring cardioversion or anticoagulation

61
Q

Ruptured AAA often results in formation of a ___, which may mask symptoms until ___.

A

Ruptured AAA often results in formation of a retroperitoneal hematoma, which may mask symptoms until the hematoma expands beyond the retroperitoneal space.

Only once the hematoma moves into the abdomen will it compress other vessels and cause symptoms.

62
Q

Treatment of acute priapism

A

Aspiration of blood from the corpora cavernosa is often the first step

Phenylephrine may also be utilized to stimulate contraction of cavernosa smooth muscle and thereby expell blood

63
Q

Mitral stenosis and pregnancy

A

Mitral stenosis is a high-risk disease during pregnancy

Therefore, intervention should be attempted prior to becoming pregnant

64
Q

Indications for mitral valve repair in MR

A
  • Secondary MR: Medical problem, no surgery
  • Primary MR:
    • LVEF 30-60% (regardless of symptoms)
65
Q

Local vascular complications of cardiac catheterization

A
66
Q

The great majority of cardiax myxomas arise in. . .

A

. . . the left atrium

67
Q

Afebrile flank pain and hypotension which develop acutely with associated syncope

A

Suspicious for AAA rupture

68
Q

When to stent vs when to CABG in CAD?

A
  • 1-2 vessels that are out on the periphery: Stent + clopidogrel
  • Left main stem, Left main stem equivalent (both LCA and LAD), or 3+ vessels: CABG
69
Q

What vessels do we use for CABG?

A

Left internal mammary artery for most important lesion

Saphenous vein graft for all other vessels

70
Q

“Hard signs” of vascular injury and what to do about them

A
  • Signs:
    • Pulsatile bleeding
    • Thrills or bruits over the injury
    • Expanding hematoma
    • Exam signs of distal ischemia (cool, weak pulses)
  • What to do:
    • Surgery. No waiting, no diagnostic tests, just GO TO SURGERY

Surgery Clerkship (42 decks)

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