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First sign on arterial waveform of occlusive disease

Loss of dicrotic notch

Dilatation of artery <50% of normal diameter

Ectasia

Dilatation of artery >50% of normal diameter

Aneurysm

Diffuse arterial enlargement >50% with no discrete aneurysms

Arteriomegaly

Multiple discrete aneurysms

Aneurysmosis

False or pseudoaneurysms

Do not contain all three layers of arterial wall

Most common site of false or pseudoaneurysms

Femoral (usually iatrogenic following use of percutaneous femoral and upper extremity access to perform diagnostic and interventional procedures)

Treatment of false or pseudoaneurysms

1. Small (<1.0 cm) FAs may spontaneously thrombose
2. Ultrasound-guided thrombin injection (UGTI) (success rates greater than 95% in most reported series) [for ones >2cm]
3. Ultrasound-guided compression
4. Open repair [in patients that have active bleeding, overlying skin necrosis, distal limb ischemia, nerve deficits from compression, and large aneurysm > 5cm with wide necks]

Pathophysiology of aneurysms

1. ↓quantities of elastin and collagen
2. Imbalance between wall proteases and anti-proteases
3. Congenital collagen structural deficiencies

Congenital collagen structural deficiencies

1. Marfan's syndrome
2. Ehlers-Danlos syndrome
3. Loeys Dietz syndrome

Most common location of AAA

Infrarenal aorta

Most common etiology of AAA

Atherosclerosis (with degeneration of the medial layer)

Crawford's classification of AAA

I. Infrarenal
2. Juxtarenal
3. Pararenal
4. Suprarenal (extend above the renal arteries and correspond with the type IV thoracoabdominal aneurysm)

Positive risk factors for developing AAA

Age, gender (male>female), race (white>black), tobacco use, and a family history (1st degree relatives) of aneurysmal disease; PAD and high cholesterol; COPD

Negative risk factors for developing AAA

1. Race (black)
2. Gender (female)
3. Diabetes mellitus (1:2)

Natural history of AAA

Continuous expansion

Most frequent and lethal complication of AAAs

Rupture is the most frequent and lethal complication of AAAs

Average rate of growth of AAA

0.4 cm/year

Size and risk for rupture. Annual vs. 5 years

Annual risk for rupture
4.0~5.4 cm - 0.5% to 1%
5.5~6.0 cm - 5% and 10%
6.0~7.0 cm - 10% to 20%

5-year risk for rupture
5 cm - 25%
6 cm - 40%
7 cm - 60%
8 cm - 80%

Growth rate that is high risk for AAA rupture

>0.6 cm/yr

Clinical presentation of AAA

1. Incidental palpation of a pulsatile abdominal mass on physical exam
2. Symptoms may be caused by contained or free rupture of the aneurysm, by thrombosis, or by distal embolism
3. Classic triad of sudden-onset midabdominal or flank pain, shock, and the presence of a pulsatile abdominal mass (1/3 of patients)

Diagnostic studies of AAA

1. Physical exam
2. Abdominal U/S
3. Spiral CT scanners with multiplanar views and three-dimensional CT angiography (CTA) *
4. MRI (modality of choice for patients with AAA who have renal insufficiency)/MRA
5. Contrast arteriography

Preferred method of screening for AAA

U/S: reduction in AAA-related mortality ranging from 21% to 68% as well as a 45% to 49% reduction in the incidence of ruptured AAA.

_____ and _____ are predictors of AAA expansion and rupture, especially for large aneurysms

Diastolic HTN; severe COPD

Indications for repair of AAA

1. >5 cm (female) or >5.5 cm (male)
2. Rapidly expanding (>0.5 cm/yr)
3. Symptomatic/ruptured
4. Atypical aneurysms (dissecting, pseudoaneurysms, mycotic, saccular, and penetrating ulcers) regardless of size
+ presence of cerebrovascular or COPD

Techniques of open repair for AAA

1. Transperitoneal approach, through a long midline incision or through a mini-laparotomy
2. Retroperitoneal approach through a left flank incision.

Complications following elective open aortic aneurysm repair

1. Nonfatal myocardial infarction, 3.1% to 16% (average 6.9%), usually within the first 48 hours after surgery.
2. Renal failure is the second most frequent complication (markedly increases mortality)
3. Post-operative bleeding
4. Most serious gastrointestinal complication is ischemia of the left colon and rectum
5. Lower extremity ischemia may result from embolization of mural thrombus or atherosclerotic plaque from the aneurysm, or thrombosis distal to the vascular clamp
6. Postoperative sexual dysfunction in males is more frequent and is due to injury to the autonomic nerves during para-aortic dissection and dissection of the iliac arteries (retrograde ejaculation & loss of potency)
7. DVT

Most significant predictors of mortality of AAA are the presence of _____ and _____

Pre-op hypotension
Low hematocrit

Other factors:
age
intraperitoneal rupture
transfusion requirements
gender (F>M)

#1 cause of acute death after AAA surgery

MI

#1 cause of late death after AAA surgery

Renal failure

Graft infection rate following AAA repair

1%

Most common late complication after aortic graft placement

Atherosclerotic occlusion

Bloody diarrhea after AAA, you must worry about ...

Ischemic colitis

Major vein injury with proximal cross-clamp during AAA repair

Retroaortic renal vein

Mortality with elective AAA repair

3-5%

Indications for re-implantation of IMA following aortic bypass (AAA repair)

Mandatory
- Previous colon resection

Relative
- Backpressure < 40 mmHg (poor backbleeding)
- SMA stenosis
- Large meandering artery with retrograde flow
- Loss of Doppler signal in mesentery
- Clinical ischemia (flow to left colon appears inadequate)

How do you avoid vasculogenic impotence during repair of AAA

Maintain flow to at least one internal iliac atery

Most important factor in survival following ruptured aneurysm

Time to clamping/occluding the aorta

Overall mortality following ruptured aneurysms

>90%

Ideal criteria for EVAR

1. Neck length >15mm (proximal) >10mm (distal)
2. Neck diameter <30mm
3. Neck angulation <60°
4. Common iliac artery length >35mm
5. Common iliac artery diameter <22mm
6. Nontortuous, noncalcified iliac arteres
7. Lack of neck thrombus

Endoleak Type I

Leakage around the proximal neck (IA) or the distal iliac end (IB). This leak is usually identified at the completion angiogram during the procedure and requires immediate repair.

Tx: Balloon the endograft again - if this is unsuccessful, an extension aortic cuff is placed proximally (IA) or an iliac limb extension is placed distally (IB)

Endoleak Type II

Blood flow into the aneurysm sac due to opposing blood flow from collateral vessels (patent lumbar arteries, inferior mesenteric artery, or hypogastric arteries)

Endoleak Type III

Leakage from overlap sites (IIIa) or through a defect in the endograft material (IIIb) [endograft components].

*This leak is becoming uncommon because of the continuous improvement in device design and because we now know that at least 2 to 3 cm of overlap are required

Tx: Secondary graft (immediately)

Endoleak Type IV

Endotension: sac continues to expand without any of the previously described endoleaks on thin-cut CT scan and angiogram → endograft acts as a filter, allowing serum to leak through and filtering most of the cells.

Tx: Secondary stenting (nonporous) or observe

AAA (elective) + intraabdominal malignancy

Patients with AAAs >5 cm and concomitant CRC, a synchronous operation may be the best approach (bowel resection with loop colostomy)

Patients with AAAs <5 cm and concomitant CRC might best be treated with colonic resection first , followed by staged AAA repair.

AAA (elective) + cholelithiasis

Avoid prophylactic cholecystectomy at the time of open repair and believe that the patient ought to be managed expectantly with a low-fat diet and possibly medication such as ursodiol in the postoperative period

What is inflammatory aneurysm?

Occurs in 5-10% of AAA, typically have a dense fibrous, inflammatory rind that is usually adherent to the 3rd and 4th portions of the duodenum and often involves the inferior vena cava and left renal vein; ureteral entrapment in 25%

*Diagnosis is best made by CT and CTA, with four separate layers typically identified: aortic lumen, mural thrombus, thickened aortic wall, periaortic inflammatory tissue.

**Male preponderance; process is believed to be autoimmune

Clinical presentation(s) of inflammatory aneurysms

- Abdominal or flank pain
- Associated weight loss
- ESR significantly elevated (75%)

Operative strategy for inflammatory AAA

Proximal aortic control above the left renal vein; use ureteral catheters if the inflammatory process extends to the iliac vessels → aneurysmorrhaphy with graft placement WITHOUT dissecting off adherent structures (i.e. duodenum) and AVOID ureterolysis is possible

[inflammatory process gradually resolves with ESR returning to normal]

Most common venous anomalies encountered during open AAA repair in order

- Left-sided vena cava (0.5%)
- Retroaortic left renal vein
- Circumaortic venous collar (two renal veins encircling the aorta-6%)
- Double inferior vena cava (lying on each side of the aorta-3%)

AAA + horseshoe kidney

Its association with AAA is rare, but it complicates graft replacement because the kidney mass is usually fused anterior to the aorta. The collecting system and ureters are displaced inferiorly, and there are often multiple or anomalous renal arteries arising from the aorta

Tx: left retroperitoneal approach is advocated because it allows easier management of the multiple accessory renal arteries.

Endovascular repair is difficult or not possible because of multiple renal arteries.

Indications for retroperitoneal approach to the infrarenal aorta

1. "Hostile abdomen" (from multiple transabdominal procedures
2. Presence of enteric or urinary stomas
3. Presence of ascites
4. Presence of peritoneal dialysis catheters
5. Morbid obesity
6. Inflammatory aneurysms
7. Horseshoe kidney

Most common organisms causing mycotic aneurysms include:

Salmonella species (#1; 40%), Staphylococcus aureus (#2), and Escherichia coli

*Infections with gram-negative organisms are less common but are associated with a higher incidence of aneurysm rupture

Infected (mycotic) aneurysms account for ____ % of all AAA cases

0.1 to 1.5%

Most common symptoms in patients with infected (mycotic) aneurysms

Fever
Abdominal or back pain

Common locations of mycotic aneurysms

Femoral artery
Aorta

Diagnostic approach to mycotic aneurysms

Blood cultures, local wound culture, and indium-labeled white blood cell scan, may be needed.

Treatment of mycotic aneurysms

Surgical treatment usually includes resection and replacement with a prosthetic interposition graft via extra-anatomic bypass.

An attempt is always made to revascularize the profunda femoris artery as well (fem-fem). In an infected field, reconstruction with femoral or saphenous vein graft or rifampin-soaked prosthetic graft is an option.

Revascularization of the limb with an obturator bypass or an extra-anatomic axillofemoral or axillopopliteal bypass can also be considered.

Etiology of aortoenteric fistula

Primary aortoduodenal fistulas are rare lesions developing in up to 1% of aortic graft cases (usually occurs >6 months after surgery

Presentation of aortoenteric fistula

Aortoenteric fistula is considered in all patients with GI hemorrhage with a known abdominal aortic aneurysm or a previous prosthetic aneurysm repair. Hemorrhage in this situation is often massive and fatal unless immediate surgical intervention is undertaken.

Typically, patients with bleeding from an aortoenteric fistula will present first with a "sentinel bleed." This is a self-limited episode (with hematemesis) that heralds the subsequent massive, and often fatal, hemorrhage.

Therapy of aortoenteric fistula

Ligation of the aorta proximal to the graft, removal of the infected prosthesis, and extra-anatomic bypass

Most common organisms causing prosthetic aortic graft infections

1. Staphylococcus (#1) -- epidermidis or aureus
2. E. coli (#2)

Most common complications of aneurysm below inguinal ligament

Thrombosis and emboli

Most common peripheral aneurysm

Popliteal aneurysm

Almost all patients (97%) with PAAs are (male or female), and the disease is bilateral in ____ %

Male; 50-70%

Patients with PAAs are at high risk for ...

Thromboembolism (embolization > thrombosis) with limb ischemia

Indication for PAA repair

1. >2 cm
2. Symptomatic [tibial nerve compression or popliteal v. thrombosis]
3. Mycotic

Approach to PAAs when no runoff vessels are seen on CTA/angiogram

Thrombolytics

When patient is diagnosed with PAAs, what the next step in diagnosis?

Rule out aneurysm elsewhere - AAA, femoral, etc.

Treatment of PAAs

Exclusion (proximal and distal ligation) and bypass of all poplitealaneurysms

What accounts for 90% of peripheral aneurysms?

Popliteal and femoral aneurysms

____% of patients have a concomitant aortoiliac aneurysm

>90%

How does FAAs (common and SFA aneurysms) behave

All true FAAs larger than 2 cm need to be considered for repair because of either risk for thromboembolic complications or an increased risk for rupture

FAA involving _________ artery has high risk of rupture

Profunda femoris (50%)

Treatment of FAAs

Bypass with exclusion

Idiopathic non-atherosclerotic lesions of arterial wall with alternating stenoses and small aneurysms

Fibromuscular dysplasia

"String of beads" finding on CT-A/angio and duplex US

Most common variant of fibromuscular dysplasia

Medial fibrodysplasia

Most commonly involved vessels

Renal (right) > carotid > iliac

[Subclavian and mesenteric vessels are not involved]

Incidence of intracranial aneurysms in patients with FMD

23%

Classic appearance on angiography of fibromuscular dysplasia

String of beads

Typical patient with FMD

Young female (multiparous) +/- HTN (if renal artery involved)

Treatment of FMD

PTA (1st choice) vs. bypass vs. open arteriotomy and serial dilation

Typical macroscopic morphology of renal artery aneurysms

Most are saccular, and 75% occur at the bifurcation of the primary or secondary branches

Most common etiology of renal artery aneurysms

Medial fibroplasia/degeneration is the most frequent cause of true renal aneurysms, followed by degenerative atherosclerosis and polyarteritis nodosa

Most frequent cause of false renal aneurysms

Spontaneous or traumatic dissection

Clinical presentation of patients with RAAs

Patients are usually asymptomatic or have associated renal artery occlusive disease and renovascular hypertension or ischemic nephropathy. Rupture occurs in less than 3% of cases

Indications for surgical repair of RAAs

Any aneurysm >2 cm in a woman of childbearing age (when the aneurysm ruptures in a pregnant woman, the fetal mortality rate is 75%, and the maternal mortality rate is 50%) should be repaired; symptomatic, expansion, >1.5 cm

Treatment of RAAs

Reconstruction with vein patch; nephrectomy if rupture occurs

Disease of intima

Atherosclerosis

Disease of media

HTN

Large vesel vasculitis

1. Temporal arteritis (giant cell arteritis)
2. Takayasu's arteritis

Typical patient population of temporal arteritis

Patients older than 50 years of age, with a slight (2 : 1) female preponderance.

Clinical presentation(s) of temporal arteritis

There are often signs of systemic inflammation (fever, myalgias). Ischemic symptoms are common, including claudication of facial or extremity muscles and retinal ischemia. Headache is a common symptom. Blindness, usually irreversible, is a dreaded complication if left untreated.

Treatment of temporal arteritis

When the clinical diagnosis is suspected, treatment must be prompt and consists of high-dose corticosteroid therapy.

Takayasu's arteritis is also known as ...

Pulseless disease

Typical patient population of Takayasu's arteritis

Younger female patients (85%) and has a higher prevalence in those of Eastern European or Asian descent.

4 types of Takayasu's arteritis

1. Aortic arch and arch vessels (brachiocephalic vessels of the arch)
2. Descending thoracic and abdominal aorta
3. Arch vessels and abdominal aorta & branches (65%)
4. Primarily pulmonary involvement (15%)

The arterial pathology of Takayasu's arteritis is focused on which vessel(s)?

Aorta (arch) and its major branches; pulmonary artery

Treatment of large vessel vasculitis

Steroids; bypass of large vessels if needed ( indicated for ischemic manifestations and is only undertaken when active inflammation is under control; normalized ESR)

NO endarterectomy

Phases of radiation arteritis

1. Early - sloughing and thrombosis (obliterative endarteritis)
2. Late (1~10 years) → fibrosis, scar, stenosis
3. Late-late (3~30 years) → advanced atherosclerosis

Pathophysiology of radiation-induced arteritis

Intimal proliferation and thickening; medial hyalinization; cellular infiltration of adventitia

Treatment of radiation-induced arterial damage

Standard surgical techniques - avoid prosthetic grafts; use vein graft

Types of medium arteritis

1. Polyarteritis nodosa
2. Kawasaki's disease (pediatric)
3. Drug abuse arteritis

Treatment for polyarteritis nodosa

Steroid +/- cyclophosphamide therapy

What type of lesions does polyarteritis nodosa cause and location?

Focal necrotizing lesions; medium muscular arteries

Polyarteritis nodosa commonly involved which organs

1. Kidney
2. Liver
3. GI tract
4. Heart

Complications secondary to polyarteritis nodosa

Formation of aneurysms in multiple areas that rupture or thrombose

Febrile exanthematous illness that affect children

Kawasaki's disease

Patients with Kawasaki's disease commonly die from ____

Cardiac conditions (arrhythmias or MI)

Kawasaki's disease is associated with what types of vascular lesions

Dilated coronaries and brachiocephalic vessels (>20%)

Treatment for Kawasaki's disease

Steroids +/- CABG

Iritis associated with oral and genital ulcers

Behçet's

Most common vascular disorder associated with Behçet's disease

Venous thrombosis (12-27%)

Once DVT develops in Behçet's, the patient must go on what ____

Life-long anticoagulation

Surgical repair of Behçet's is associated with ___

↑Thrombosis, pseudoaneurysm

Treatment of Behçet's

Steroids & immunosuppressive agents

Behçet's is commonly found in what regions of the world

Middle East and Asia (Turkey)

Types of small vessel arteritis

1. Hypersensitivity vasculitis
2. Buerger's disease (thromboangiitis obliterans)

Conditions associated with hypersensitivity vasculitis

Henoch-Schonlein purpura
Cryoglobulinemia

Clinical presentation of Buerger's disease

Young male smoker who presents with severe distal medium to small arterial disease → severe rest pain with bilateral ulceration OR ischemia or gangrene of digits

*Rare in African-Americans

Feature on angiogram that is suggestive of Buerger's disease

Corkscrew vessels/collaterals

Associated condition of Buerger's disease elicited from history

Superficial migratory thrombophlebitis
Raynaud's syndrome

Treatment of Buerger's disease

Cessation of smoking
+/- Pletal
+/- Limb amputation

Leg compartments

Anterior
Lateral
Deep Posterior
Superficial Posterior

Nerve of the anterior compartment and what does it innervate

Deep fibular (peroneal) nerve → dorsiflexion of anterior compartment muscles and sensation between 1st and 2nd toes

What artery does deep peroneal nerve run along with

Anterior tibial artery

Nerve of the lateral compartment and what does it innervate

Superficial peroneal nerve → eversion, lateral foot sensation

Arteries that travels in the lateral compartment

Anterior and posterior tibial branches of the popliteal artery

Nerve of the deep posterior compartment and what does it innervate

Tibial nerve → plantarflexion

Arterial supply of deep posterior compartment

Posterior tibial artery
Peroneal artery

Most common cause of PVD

Atherosclerosis

Signs of PVD

Pallor
Dependent rubor (redness of the feet) caused by
reactive hyperemia
Hair loss
Abnormal nail growth/nail brittleness
Slow capillary refill
Muscle wasting/atrophy
Thinning of skin

#1 preventative agent for atherosclerosis

Statin drugs

What inherited disorder that affects the metabolism of the amino acid methionine ↑risk of atherosclerosis

Homocystinuria

Treatment: Folate, B₆, B₁₂

2 broad categories of PVD patients based on symptomatology

Claudication vs.
Critical limb ischemia

Define claudication

Reproducible ischemic muscle pain 2° inadequate O₂ delivery during exercise with relief soon after cessation of activity

% of patients with claudication that progress to CLI over their lifetime

5 to 10%

Annual rate of mortality in patients with claudication

2 to 5%

Annual rate of limb loss in patients with claudication; 5-year risk for loss of limb

1%; 5 %

Annual rate of gangrene in patients with claudication

2%

Most common atherosclerotic disease pattern encountered distal to the inguinal ligment

Short-segment total occlusion of the SFA (distal > proximal)

Symptoms and relation to the level of occlusion

Occur one level below the occlusion
- Aortoiliac disease → buttock claudication
- External iliac disease → midthigh claudication
- CFA/pSFA disease → calf claudication
- dSFA/popliteal disease → foot claudication

Define critical limb ischemia

Presence of rest pain or tissue loss in the lower limb

When does rest pain occur?

When blood flow is inadequate to meet resting metabolic requirements → in the LE, ischemic rest pain is localized to the foot (frequently in the instep; usually centered over the metatarsal heads, not the toes)

The severe discomfort in the forefoot usually wakes patient from sleep (at night) → temporary symptomatic relief from hanging affected extremity over the edge of the bed [walking, standing, or sleeping in a chair may relief the pain]

% of patients with CLI who will die at 1 year

25%

% of patients with CLI who will undergo major amputation

30%

% of patients with CLI who will be alive with 2 limbs

45%

Treatment for CLI

Revascularization for limb salvage

What condition can mimic claudication?

Lumbar stenosis or nerve root compression (usually develops when patients maintain a stationary standing posture)

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