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
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
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
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)
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
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
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.
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.
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.
10
Q
Differentiating claudiation pain from spinal stenosis
A
- Claudication: Of distal extremities, non-positional pain
- Spinal stenosis: “Claudication” of buttocks, positional pain
11
Q
Subtle physical exam findings of peripheral vascular disease
A
- Shiny shins
- Loss of hair
- Decreased pulse
- Lower temperature
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.
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.
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
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.
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
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
18
Q
Characteristic imaging feature of IgA vasculitis (aka Berger’s disease)
A
Corkscrew collaterals
19
Q
5 P’s of compartment syndrome
A
- Pain
- Parathesias
- Paralysis
- Pulselessness
- Poikilothermia (cold)
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.
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
22
Q
Leriche syndrome
A
- Triad of buttock / thigh claudication, impotence, and diminished femoral pulses
- This indicates iliac artery occlusive disease in a male
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.
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.
25
Treatment for arterial thromboembolism to distal extremity (in the setting of afib)
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.
26
Distinguishing vascular and neurogenic claudication
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**
27
Criteria for AAA repair
* 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)
28
If an AAA does not meet criteria for repair, you. . . .
. . . **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
29
Risk modification for control of AAA expansion
* AAA expansion can be minimized by controlling:
* Hyperlipidemia
* Hypertension
* CAD
30
Inherited conditions associated with aneurysm development
* Marfan syndrome (Fibrillin)
* Ehlers-Danlos syndrome (Type V collagen)
* Familial Thoracic Aneruysm and Dissection syndrome (aka TAAD syndrome)
31
USPSTF AAA screening recommendations
* 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
Endoleaks following EVAR
**Persistence of bloodflow outside of the endocraft** following EVAR (endovascular aneurysm repair).
Endoleaks are the most common reason for secondary intervention after EVAR.
33
Types of endoleak
* **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
Best predictors of AAA rupture
* Size
* Symptoms
35
Most AAAs are located. . .
. . . **in the infrarenal aorta**
36
Monitoring following EVAR vs open repair
* **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
Anyone diagnosed with AAA should have an exam to. . .
. . . **assess for aneurysmal disease at other locations**
38
AAAs are papable in the \_\_\_
Iliac aneurysms are palpable in the \_\_\_
AAAs are papable in the **epigastrium**
Iliac aneurysms are palpable in the **infraumbilical region**
39
While the risk of AAA is higher in \_\_\_, the risk of rupture of an existing AAA is higher in \_\_\_.
While the risk of AAA is higher in **men**, the risk of rupture of an existing AAA is higher in **women**.
40
Triad of mesenteric ischemia
* Postprandial pain
* Food fear
* Unintentional weight loss
41
Presentation of acute mesenteric ischemia
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
Vascular blood supply of the mesenteric vessels
43
SMA thrombosis vs SMA embolism
* **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
Chronic mesenteric ischemia generally only becomes symptomatic after \_\_\_
Chronic mesenteric ischemia generally only becomes symptomatic after **multiple vessels are involved**
Since there is so much collateral bloodflow in the mesentery
45
Nonocclusive mesenteric ischemia
* 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
Median arcuate ligament syndrome
* 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
Watershed regions of the intestinal tract
**The splenic flexure** (between SMA and IMA distributions)
**The mid-low rectum** (between IMA and rectal artery distributions)
48
A patient with chronic mesenteric ischemia almost always has \_\_\_
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
Chronic mesenteric ischemia is much more common in ___ than \_\_\_.
It is believed that this is due to \_\_\_.
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
Patient presents with TIA and is found to have bilateral carotid stenoses \>80%. What are the next steps in management?
* **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
When do we intervene on patients with carotid stenosis
* \>50% with symptoms (TIA, stroke)
* \>60% without symptoms
52
Amaurosis fugax
* "fleeting darkness" in Greek
* Temporary blindness caused by TIA
53
Carotid artery stenting
* Done percutaneously
* Carries risk of intraoperational stroke -- therefore usually done with cerebral protection devices downstream in the carotid
54
CEA or medical management for carotid stenosis
CEA ***always*** carries a lower risk long-term, but the degree of risk reduction relative to medical management varies
55
\_\_% of patients with carotid bruits on exam have carotid stenosis \> 30%
**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
Role of CT angiography, MR angiography, and catheter-based angiography in carotid stenosis
* **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
In patients who are very poor surgical candidates, specifically those with refractory CHF, ___ may be preferred for treatment of carotid stenosis
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
Complete internal carotid artery occlusion
These patients are **not** **candidates for carotid endarterectomy**
59
Major perioperative complications of CEA
* **Stroke** (obviously)
* **Myocardial Infarct** (not so obvious. Unclear why this is the case, but empirically it does happen)
60
Post-CABG atrial fibrillation
Common and self-limited
Resolution is typically within 24 hours, not requiring cardioversion or anticoagulation
61
Ruptured AAA often results in formation of a \_\_\_, which may mask symptoms until \_\_\_.
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
Treatment of acute priapism
**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
Mitral stenosis and pregnancy
Mitral stenosis is a high-risk disease during pregnancy
Therefore, intervention should be attempted prior to becoming pregnant
64
Indications for mitral valve repair in MR
* Secondary MR: Medical problem, no surgery
* Primary MR:
* LVEF 30-60% (regardless of symptoms)
65
Local vascular complications of cardiac catheterization
66
The great majority of cardiax myxomas arise in. . .
. . . **the left atrium**
67
Afebrile flank pain and hypotension which develop acutely with associated syncope
Suspicious for AAA rupture
68
When to stent vs when to CABG in CAD?
* **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
What vessels do we use for CABG?
**Left internal mammary artery** for **most important lesion**
**Saphenous vein** graft for **all other vessels**
70
"Hard signs" of vascular injury and what to do about them
* 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**
