NOSM VASCULAR RESOURCE

vascular medicine , surgery and wound care

Table of Contents
Visceral artery aneurysms
Visceral artery aneurysms
The incidence of is approximately 0.01% to 2% in autopsy and angiographic studies .Multiple aneurysms are present in approximately one third of patients 

splenic artery > 50%
hepatic artery 20% and increasing with interventions
superior mesenteric 6%
coeliac artery 4%
gastro/epiploic artery 4%
pancreatic/duodenal artery 4%
small bowel artery 3%
inferior mesenteric artery 1%

True visceral artery aneurysms are secondary to vessel wall degeneration, and demonstrate deficiency of the arterial media with loss and/or fragmentation of the elastic fibers and reduced smooth muscle. Arteriosclerosis, congenital syndromes, fibromuscular dysplasia, gestational alterations, and collagen disorders are other possible causes.

Pseudoaneurysms can develop as a result of blunt or penetrating trauma, inflammation, infection, vasculitis, and iatrogenic trauma secondary to surgical, endoscopic, and radiologic procedures.


Both visceral artery aneurysms and pseudoaneurysms frequently present as life-threatening emergencies. Both are now being diagnosed with increasing frequency, related to routine use of magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound. Both surgery as well as endovascular techniques are used. The endovascular route is much more common and includes transarterial deployment of coils, N-butyl cyanoacrylate, or stent grafts. Direct percutaneous embolization of visceral aneurysms and pseudoaneurysms may also be performed. Percutaneous endovascular management, now offers a safe and effective alternative to conventional surgery with lower procedural morbidity and mortality and high technical success rates.This is borne out in the author's own personal experience treating surgically hepatic artery, splenic artery, inferior and pancreatic artery aneurysms which now would simply be done by endovascular approach as an outpatient procedure


T
ypically, surgery or endovascular management is considered for VAAs when they are larger than 2 cm in diameter, demonstrate rapid growth, and when patients present with symptoms attributable to the aneurysm.

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Review

Definition: bulging or dilatation of native aorta > 3 cm
generally 2X normal size
described as saccular or fusiform, the former more likely to rupture earlier


RISK FACTORS

Sex: Men develop AAA four to five times more often than women.


Age: Rises with age >65
2-13% men vs 6% women >65
Most picked up by screening are small <4cm

Family history: male sibling >60,18%

Smoking:

PAD, CAD, hpertension:


Screening


Screening: by ultrasound

All men,65-75 who ever smoked
All men >60 with family history

Generally women are not screened unless there is a family history or who have evidence of PVD or CAD


Definitive investigation is by CT scan particularly when US >5.5cm


Only 30% detection by clinical exam, the rest by imaging



Risk of rupture

Less than 4.0 cm in diameter = less than 0.5 percent

Between 4.0 to 4.9 cm in diameter = 0.5 to 5 percent

Between 5.0 to 5.9 cm in diameter = 3 to 15 percent

Between 6.0 to 6.9 cm in diameter = 10 to 20 percent

Between 7.0 to 7.9 cm in diameter = 20 to 40 percent

Greater than or equal to 8.0 cm in diameter = 30 to 50 percent

The risk of rupture of large aneurysms (≥5.0 cm) is significantly greater in women than men .
Aneurysms expand at an average rate of 0.3 to 0.4 cm/year. Aneurysms that expand rapidly, more than 0.5 cm over six months are at high risk of rupture.

AAA can rupture, become inflamed or infected, be a source of thromboembolism or fistulize into bowel or vein


Treatment

Generally at 5.5 cm by CT measurement

T
he majority of infrarenal AAA are stented unless there is hostile anatomy such as angle of neck, length of neck ,thrombus, calcification, size of landing vessels, or compromised internal iliac arteries.Aneurysms are still done open pending patient preference, age or hostile anatomy.The higher the patient risk the harder to safely do a stent repair!




This patient was riddled with aneurysmal disease He had previous AAA repair ,carotid aneurysm repair, popliteal aneurysms bilaterally. While on dialysis he developed brachial and AV aneurysms.Pictured below is the arterialized aneurysm which developed in his saphenous vein conduit for one of the popliteal aneurysms
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Asymptomatic disease

This author tends to be conservative.Medical physicians tend to support this position since current guidelines are based on older studies which do not reflect optimal best management, particularly statin management, anticoagulation, cardiac and BP control.

The previously touted stroke and death rates post intervention are found only in centres of excellence with high volumes.There is great surgeon and institution variation.

It is important to identify the high risk asymptomatic patient who may be in need of an intervention.Certain clinical features might include male smokers with poorly controlled hypertension and a previous TIA/stroke on the opposite side.

Risk stratification might be based on indirect degree of stenosis but more importantly progression of that stenosis.Previous infarcts found on the ipsilateral side on CT as well as worrisome plaque characteristics such as ulcers, echolucency are signs of increasing probability of future mischief.

Some feel women and the elderly get the least benefit in the asymptomatic group with either surgery or stent

Using the intent total model, eight carotid endarterectomies are needed to prevent one stroke vs 20 in the asymptomatic group using absolute reduction rates over five years.The absolute reduction rate for one year is is only 1%,therefore is 100 endarterectomies in one year to prevent one stroke



Screening

Ultrasound assessment of carotid arterial atherosclerotic disease has become the first choice for  screening, permitting the evaluation of both the macroscopic appearance of plaques as well as flow characteristics in the carotid artery.


Society of Radiologists in Ultrasound (SRU) consensus
This consensus developed recommendations for the diagnosis and stratification of ICA stenosis .
[PSV = peak systolic velocity; EDV = end diastolic velocity; ICA = internal carotid artery; CCA = common carotid artery]


  • normal:
    • ICA PSV is <125 cm/sec and no plaque or intimal thickening is visible
    • additional criteria include ICA/CCA PSV ratio <2.0 and ICA EDV <40 cm/sec
  • <50% ICA stenosis:
    • ICA PSV is <125 cm/sec and plaque or intimal thickening is visible
    • additional criteria include ICA/CCA PSV ratio <2.0 and ICA EDV <40 cm/sec
  • 50-69% ICA stenosis
    • ICA PSV is 125-230 cm/sec and plaque is visible
    • additional criteria include ICA/CCA PSV ratio of 2.0-4.0 and ICA EDV of 40-100 cm/sec
  • ≥70% ICA stenosis but less than near occlusion:
    • ICA PSV is >230 cm/sec and visible plaque and luminal narrowing are seen at gray-scale and colour Doppler ultrasound (the higher the Doppler parameters lie above the threshold of 230 cm/sec, the greater the likelihood of severe disease)
    • additional criteria include ICA/CCA PSV ratio >4 and ICA EDV >100 cm/sec
  • near occlusion of the ICA:
    • velocity parameters may not apply, since velocities may be high, low, or undetectable
    • diagnosis is established primarily by demonstrating a markedly narrowed lumen at colour or power Doppler ultrasound
  • total occlusion of the ICA:
    • no detectable patent lumen at gray-scale US and no flow with spectral, power, and colour Doppler ultrasound
    • there may be compensatory increased velocity in the contralateral carotid
    • If indicated this may be followed up with a CTango,MR angio or catheter based angio which is now rarely do
    • Factors leaning toward carotid stent vs open CEA would include:
  • Low carotid lesion (suggested by low common carotid artery [CCA] velocities)
  • High carotid lesion (above C2)
  • Previous carotid endarterectomy (CEA)
  • History of other major neck operation or tracheostomy
  • Cervical fusion
  • Poor neck mobility
  • Previous neck irradiation
  • Symptomatic disease
  • < 50% treated by best medical management
  • 50-60% treated on individual situation
  • > 60% best treated by intervention
  • Treatment by stenting or surgery
  • Statistically equal but recurrence rate is higher in stent group as well as post intervention neurological events. Surgery does have a higher MI rate.
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Fortunately rare, occurring in less than 5% of reconstructions, aorto enteric fistulas are life threatening.They are associated with high mortality and morbidity with and without treatment. Despite treatment , both limb and life are threatened with renewed graft infections.80% involve the duodenum, followed by distal small bowel then colon respectively. Stenting is a good short term solution but generally is not definitive therapy!
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Endoscopy

CT scan

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CLINICAL

For a recent overview on AEF , use the following the LINK in JACS ,July 2017
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Indications:

60% are in diabetics

gangrene or irreversibly ischemic

sepsis

pain

malfunction

trauma, particularly in young <50

male preponderance

Remember the 6 P's of AAO (acute arterial occlusion)

Pain
Palor
Paraesthesia
Paralysis
Pulselessness
Perishing with cold

The higher the level of amputation the more the energy to wear a prosthesis

Always attempt the lowest level possible particularly in the young

Types: Closed vs open(Guillotine)




Digit: (most common)
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Ray:
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Transmetatarsal amputations: (Mostly diabetics or trauma)
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Below knee: ( do if possible instead of above knee)
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Above knee: (if not bleeding go to a higher level)
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Hip disarticulation: (failed above knee)
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Rare, but useful:
Syme: (useful in children, allows growth and may ambulate without prosthesis)
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Chopart: (mid tarsal disarticulation)
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Lisfranc: (metatarsus/tarsus disarticulation)
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The Ideal Vascular Access

easily created /maintained with minimal
surgical intervention
associated with minimal personal
dysfunction
easily usable over/over again
easily monitored
receives consistent, effective cannulation
little maintenance intervention

Ideal access is AVF ,followed by graft followed by central tunnelled catheter


National Kidney Foundation

Kidney Disease Outcomes Quality Initiative
NKF/KDOQI
The gospel for clinical guidelines, best practice
and evidence-based medicine.For a more complete overview see
Dialysis Interventions in the Powerpoint section of this web site


Access types

AV fistula
AV graft
Tunneled catheter
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Major complications include infection , ischemia and aneurysms
Innovative solutions
Chronic Limb ischemia (back to top)

Limb schema if chronic shows progression from claudication to disabling claudication to rest pain to incipient gangrene then frank gangrene


Claudication is defined as a pain or discomfort in a group of muscles, usually the legs, thighs, or buttocks, that is worsened by exercise (ie, walking) and relieved with rest. Claudication literally means “to limp”
The most common cause of claudication is peripheral artery disease, less common ,aneurysm,and neurospinal disease

The diagnosis of vascular claudication is defined in the Edinburgh criteria for claudication

The severity of disease depends on the degree of narrowing plus the status of collaterals.


The major risk factors for developing PAD include hypertension, hyperlipidemia, cigarette smoking and diabetes. Smoking is public enemy Number 1. For the science on this topic see P.A.D. in the Powerpoint section of this web site. For an overview of historic and current classifications of various approaches to PAD follow this LINK



Claudication Diagnosis

The diagnosis can usually be made on history and physical exam


History

Calf pain — Calf pain is the most common complaint. It always occurs with exercise and is relieved with rest. Claudication pain in the upper two-thirds of the calf is due to disease in the superficial femoral artery), whereas pain in the lower third of the calf is due to disease in the popliteal artery.
Thigh pain — Thigh claudication often results from the narrowing of the superficial femoral artery in the upper thigh or from the common femoral artery), or iliac arteries.
Buttock pain — When symptomatic, blockage in the aorta) gives buttock, hip, or thigh pain. The pain is often described as aching, and there may also be weakness while walking up stairs. Other physical signs include loss of muscle mass and hair loss on the lower extremities. Erectile dysfunction (ED) may also occur .

Physical

Decreased or absent pulse

Bruit over abdomen or groins

Decreased range of motion to feet

Peripheral hair loss

Non healing lesions

Pallor with elevation, rubber with dependency, prolonged venous filling time


Investigation

Non invasive arterial studies which may include ankle brachial index(ABI),duplex, segmental pressures

CT angiogram, MR angiogram ,standard peripheral angiogram(usually in anticipation of an intervention).Peripheral angio should only be done with the understanding of procedure at the same setting.


Medical therapy

exercise program

behaviour modification(cigarettes)

Risk factor reduction i.e. hypertension, diabetes, lipid status, coronary artery disease and SMOKING

Medication

Cilastosol(not available in Canada)

Pentoxyphylline

Naftidrofurl (Europe)

Statins

Antiplatelet therapy(ASA, Plavix)


There is no standardized treatment for claudication

Adopt angioplasty /stent first approach

If above fails ,surgery


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Acute limb ischemia (back to top )

Definition:
a sudden decrease in limb perfusion threatening limb viability (TASC 11), manifesting as rest pain or tissue loss (ulcer or gangrene).Presentation varies with etiology and the presence of underlying PVD.Presentation after two weeks is considered chronic limb ischemia (UpToDate,2017)


ETIOLOGY

!)
Embolus from a proximal source.

Over 80% come from the heart associated with either atrial fibrillation, MI, endocarditis, valvular heart disease, atrial myxoma or prosthetic valves.
An arterial source accounts for 15-20% associated with aneurysms or atherosclerotic plaques


2) Paradoxical embolus <5%


Areas affected:

Femoral – 28 %, Arm-20%, Aorta-iliac-18%, Popliteal-17%, Visceral and other- 9%each

3) Thrombosis
Occlusion of a previously patent artery ,graft or stent often due to plaque haemorrhage or progression of the atherosclerotic process leading to stasis and thrombosis.the presenting features usually less severe than with embolus because of the presence of collaterals.Rare causes include arteries with collagen vascular disease, ergotism thrombophilia, antiphospholipid syndrome and homocysteinemia

4) Local or remote arterial dissection


5) Trauma (blunt ,penetrating or iatrogenic)



6) Low flow state


7) Massive venous obstruction
(phlemasia alba and cerulea dolens)




Clinical presentation usually involves all or part of the 6 P's depending on the status of collaterals


6 P's: Pain, Pallor, Paresthesia, Paralysis,Pulselessness and Poikilothermia

Irreversible damage after 6 hours after initial presentation


Factors favouring embolus include atrial fibrillation, acuteness, mechanical valve, pacemaker and normal pulses on opposite site

Factors favouring thrombosis include chronicity of presentation, previous revascularization surgery, history of claudication, evidence of chronic disease on opposite limb

Assessment of ischemia may be difficult

A viable limb has no sensory loss or paralysis , mild to moderate pain with both audible arterial and venous doppler assessment

A threatened limb has severe pain, minimal sensory loss, mild paralysis, severe pain ,no flow on arterial doppler, but flow on the venous doppler

A non viable,essentially dead limb, lacks arterial and venous doppler flow, anaesthesia of the limb, severe to total paralysis

It is sometimes difficult to distinguish a threatened limb from a non viable limb.Attempt at flow restoration may cause a compartment syndrome and revascularization syndrome which be a lethal complication

Investigation:

Embolus: CT angio if diagnosis not secure on clinical grounds
Echocardiogram(may be delayed until post treatment
Doppler assessment


Thrombosis: CT angio +/- standard angio
Coagulation screen +/- collagen work up
Doppler assessment

Trauma/dissection: CT angio
Doppler assessment


Viable/threatened limb versus non viable limb

Non viable needs immediate amputation at the lowest level possible

Viable/threatened limb needs immediate IV heparin bolus plus infusion pending disposition

Viable non threatened limb does not have the same urgency as a threatened limb.May need to do do standard angio if planning thrombolytic therapy followed by a catheter based intervention .Endo first approach now favoured over standard surgery if available

Thrombolytic therapy works better in an occluded graft than native vessel

Threatened limb needs immediate attention.Standard angio may be necessary especially if planning thrombolytic therapy and a catheter based intervention

A secure diagnosis of an embolus best treated by embolectomy versus thrombolytic therapy

Thrombolytic therapy is safer and more effective if given intra arterial and catheter based

Acute limb ischemia is important to diagnose because it carries a high mortality and morbidity.
Estimates of mortality following acute limb ischemia range from 9-22%

Limb salvage following acute limb ischemia is estimated at 70-90%

Amputations are more common following thrombotic occlusions, since these are more likely to occur with established peripheral arterial disease
Interestingly enough, despite improved sometimes disruptive technologies the mortality and morbidity has not changed much over the last 25 years.Please look at the author's prospective study published in 1983 and look at the amputation rates and mortality.(
Surgery.1983 Mar;93(3):381-5)

Acute limb ischemia

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Ergot poisoning

See above case history in Interesting vascular caeses

Acute ischemia (aorta to infrapopliteal arteries)

Renal artery aneurysm (back to top)

For a review of etiology and management follow this
LINK
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