CHAPTER 27- VASCULAR

resistance to activated protein C (leiden factor)

smoking

1st- foam cells --> macrophages that have absorbed fat and lipids in the vessel wall

2nd- smooth muscle cell proliferation --> caused by growth factors released from macrophages, results in wall injury

3rd- intimal disruption (from smooth muscle cell proliferation) --> leads to exposure of collagen in vessel wall and eventual thrombus formation --> fibrous plaques then form in these areas with underlying atheromas.

• Risk factors:
• 1- smoking
• 2- HTN
• 3- hypercholesterolemia
• 4- DM
• 5- hereditary factors

Atherosclerosis- disease of the intima

Hypertension- disease of the media

1) stroke is the 3rd most common cause of death in the united states

• 2) HTN- most important risk factor for stroke in asymptomatic patients
• - carotids supply 85% of blood to the brain
• - bifurcation- most common site of stenosis

3) Normal internal carotid artery has continuous forward flow

• 4) normal external carotid artery has triphasic flow
• - 1st branch of external carotid artery- superior thyroid artery
• - communication between internal carotid artery and external carotid artery with opthalmic artery (1st branch of ICA) and internal maxillary artery (off ECA)

5) Middle cerebral artery- most commonly diseased intracranial artery

• 6) cerebral ischemic events- most commonly from arterial embolization (not thrombosis) from the ICA
• - can also occur from a low-flow state through a severely stenotic lesion
• - heart 2nd most common source of emboli

7) anterior cerebral artery events- mental status changes, release, slowing

8) middle cerebral artery events- contralateral motor and speech (if dominant side); contralateral facial droop

• 9) amaurosis fugax- occlusion of the opthalmic branch of the ICA (Visual changes --> shade coming down over eyes); visual changes are transient
• - see hollenhorst plaques on opthalmologic exam

• 10) Carotid traumatic injury with major fixed deficit
• - if occluded do not repair --> can exacerbate injury with bleeding
• - if not occluded--> repair

1) should be considered in any patient with >70% stenosis and symptoms

2) asymptomatic patients with 70-80% stenosis more controversial

3) any patients with >80-90% stenosis should have CEA if technically possible

4) recent completed stroke --> wait 4-6 weeks and then perform CEA if it meets criteria (bleeding risk if performed earlier)

5) Emergent CEA may be of benefit with fluctuating neurologic symptoms or crescendo/evolving TIAs

6) shunt during CEA for stump pressures <50

7) repair the tightest side first if the patient has bilateral stenosis

8) repair the dominant side first if the patient has equally tight carotid stenosis bilaterally

1) vagus nerve- most common cranial nerve injury with CEA --> secondary to vascular clamping during endarterectomy; patients get hoarseness

2) hypoglossal nerve- tongue deviation to the side of injury--> speech and mastication difficulty

3) glossopharyngeal nerve- unlikely injury; could occur with really high carotid lesion --> causes difficulty swallowing

4) ansa cervicalis- strap muscles; no serious deficits

5) mandibular branch of the facial nerve- affects corner of mouth (smile)

6) acute event immediately after CEA--> back to OR to check for flap or thrombosis

• 7) Pseudoaneurysm- pulsatile, bleeding mass after CEA
• - treatment: nipride to avoid bleeding

8) Myocardial infarction- most common nonstroke morbidity and mortality following CEA

9) 15% restenosis rate after CEA

carotid stenting is another option compared with CEA- this new technology seems most beneficial for high-risk patients (i.e. patients w/previous CEA, medical disease that makes them too high risk for surgery, etc)

Medical comorbidity:

• 1) age >80
• 2) coronary artery disease
• 3) acute myocardial infarction in prior 4 weeks or CABG within prior 6 months
• 4) congestive heart failure (class III/IV)
• 5) Ejection fraction - 30%
• 6) dialysis dependent renal failure
• 7) severe chronic obstructive pulmonary disease
• 8) FEV1<1.01

• Local Factors
• 1) carotid restenosis after CEA
• 2) anatomically high lesion (above second vertebrae)
• 3) contralateral internal carotid artery occlusion
• 4) radiation-induced internal carotid artery stenosis
• 5) prior neck dissection
• 6) permanent tracheal stoma
• 7) cervical scarring

1) usually bilateral, at origins, usually need bilateral disease to have symptoms

2) caused by spurs, bands, trauma; get vertebrobasilar insufficiency

• 3) Symptoms:
• -diplopia
• -dysarthria
• -vertigo
• -tinnitus
• -drop attacks
• -incoordination
• -binocular vision loss

• 4) Treatment:
• 1- PTA (percutaneous transluminal angioplasty)
• 2- vertebral artery transposition to subclavian
• 3- transsubclavian endarterectomy
• 4- osteophyte resection
• 5- unroofing of transverse process foramina
• 6- resection of musculotendinous bands

1) present as a painless neck mass, usually near bifurcation, neural crest cells

Treatment: resection

1) from trauma, usually a deceleration injury

2) address other life-threatening injuries first (severe solid organ laceration, pelvic fracture with hemorrhage, etc. --> then repair aorta

3) get mediastinal widening from bridging veins and arteries, not leaking from aorta itself

4) usually tears at the ligamentum arteriosum, just distal to the left subclavian

5) use left heart bypass with repair

6) 90% of these patients die at the scene

1) usually caused by connective tissue disorders; cystic medial necrosis most common abnormality- Marfan's syndrome

2) Diagnosis- chest CT or aortography

3) Can get aortic insufficiency

4) often asymptomatic and picked up on routine CXR

5) can also get compression of vertebra (back pain), RLN (voice changes), bronchi (dyspnea or PNA), or esophagus (swallowing trouble)

6) symptomatic patients usually have CHF secondary to aortic insufficiency

• 7) Indications for repair:
• 1- acutely symptomatic
• 2- >5.5cm (with marfan's >5cm)
• 3- diameter 2x normal
• 4- rapid increase in size

1) from atherosclerosis

2) repair indications same as for ascending aortic aneurysms

3) patients will likely need to be cooled down and have circulatory arrest to perform repair

1) from atherosclerosis; can become quite large before symptoms occur

2) risk for paraplegia 5-10%

3) repair indications same as for ascending aortic aneurysms

4) reimplant intercostal vessels below T8 to help prevent paraplegia

Stanford classification- based on the presence or absence of involvement of ascending aorta

Class A- any ascending aortic involvement

Class B- descending aortic involvement only

based on the site of tear and extent of dissection.

• Type I- ascending and descending
• Type II- ascending only
• Type III- descending only

1) most start in ascending aorta

2) can mimic myocardial infarction

3) symptoms: searing-like chest pain; can have unequal pulses or BP in upper extremities

4) 95% of patients have severe HTN

• 5) Other risk factors:
• 1- marfan's syndrome
• 2- previous coarctation repair
• 3- atherosclerosis
• 4- infection (syphilis)

6) CXR- usually normal; may have widened mediastinum

7) Dx- chest CT with contrast

8) Dissection occurs in media layer of blood vessel wall

9) Aortic insufficiency occurs in 70% with acute disease, caused by annular dilatation or when aortic valve cusp is sheared off

10) can also have occlusion of the coronaries and major aortic branches

11) death with ascending aortic dissection usually secondary to cardiac failure from aortic insufficiency or tamponade; can also have rupture

12) Medical treatment if possible --> control blood pressure with hydralazine and beta-blockers

• 13) surgery aims at obliterating the false lumen and placing graft
• 1- operate on all ascending aortic dissections
• 2- operate on descending aortic dissection with visceral, renal, or leg ischemia, persistant pain; large size (from aortic dilatation after dissection).
• 3- need to follow these patients with lifetime serial CT scans; 30% will eventually get aneurysm formation requiring surgery

• 14) postop complications for thoracic aortic surgery:
• 1- MI
• 2- renal failure
• 3- paraplegia (especially descending thoracic aortic surgery)

15) paraplegia caused by ischemia due to occlusion of the intercostal arteries and artery of Adamkiewicz during repair

• 1) normal aorta: 2-3cm
• 2) aneurysms form from degeneration of the medial layer
• 3) most commonly due to atherosclerosis
• 4) usually found incidentally

• 5) risk factors:
• 1- HTN
• 2- male gender
• 3- smoking
• 4- elderly age

• 6) Can present with:
• 1- rupture
• 2- distal embolization (can cause lower extremity ischemic symptoms, compression of adjacent organs)

• 7) Rupture
• 1- leading cause of death without an operation
• 2- patients often have back or abdominal pain; can have profound hypotension
• 3- diagnosis: ultrasound or abdominal CT
• 4- AAA rupture risk-
• 1- starts to rise in AAAs >5cm (5cm AAA has 15-20% 5 yr risk of rupture); >8cm--> 100% rupture risk within 5 years

8) CT shows fluid in retroperitoneal space, extraluminal contrast with rupture

9) most likely to rupture on left posterolateral wall, 2-4cm below renals

10) more likely to rupture in presence of diastolic HTN or COPD (thought to be predictors of expansion)

11) 50% mortality with rupture if patient reaches hospital alive

• Treatment
• 1- repair if symptomatic
• 2- >5cm
• 3- growth >0.5cm/yr

• 2) Reimplant IMA if:
• 1- backpressure <40mmHg (poor backbleeding)
• 2- previous colonic surgery
• 3- stenosis at SMA
• 4- flow to left colon appears inadequate

3) Ligate bleeding lumbar arteries

4) maintain flow to at least one internal iliac artery (hypogastric) to avoid vasculogenic impotence

Complications:

• 1) major vein injury with proximal cross-clamp- retroaortic renal vein
• 2) impotence in 1/3 secondary to disruption of autonomic nerves and blood flow to the pelvis
• 3) 5% mortality with elective repair
• 4) #1 cause of acute death after surgery- MI
• 5) #1 cause of late death after surgery- renal failure
• 6) graft infection rate- 1%
• 7) pseudoaneurysm after graft placement-1%
• 8) atherosclerotic occlusion- most common late complication after aortic graft placement
• 9) diarrhea (especially bloody) after AAA worrisome for ichemic colitis
• 10) inferior mesenteric arery is often sacraficed with AAA repair and can cause ischemia of the left colon
• 11) Diagnosis: endoscopic or abdominal CT; rectum spared from ischemia
• 12) if patient has peritoneal signs --> take to OR for colectomy and colostomy placement
• 13) can follow closely if no peritoneal signs

perioperative complication rates seem to be lower after endovascular repair; however, the long term outcome of endovascular repair is unknown.

Ideal Criteria for AAA Endovascular Repair

• Neck Length >15mm
• Neck Diameter <30mm
• Neck Angulation <60 degrees
• Common iliac artery length- >35mm
• Common iliac artery diameter <22mm
• Other - nontortuous, noncalcified iliac arteries, lack of neck thrombus

page 185

• 1) occurs in 10% of patients with AAA; males
• 2) adhesions to 3rd and 4th portions of the duodenum
• 3) ureteral entrapment in 25%
• 4) not secondary to infection
• 5) weight loss, increased ESR, thickened rim above calcifications on CT scan
• 6) may need to place preoperative ureteral stents
• 7) inflammatory process resolves after aortic graft placement

• 1) salmonella #1, staphylococcus #2
• 2) pain, fevers, positive blood cultures in 50%
• 3) periaortic fluid, gas, retroperitoneal soft tissue edema, lymphadenopathy
• 4) usually need extra-anatomic bypass (axillary-femoral w/femoral to femoral crossover) and resection of infrarenal aorta to clear infection
• 5) bacteria infect atherosclerotic plaque, cause aneurysm

• 1) staphylococcus #1, e.coli #2
• 2) see fluid, gas, thickening around graft
• 3) blood cultures negative in many patients
• 4) treatment of choice is to resect the graft and bypass through noncontaminated field
• 5) more common with grafts going to groin (aortobifemoral grafts)

• 1) usually occurs >6months after surgery
• 2) herald bleed with hematemesis, then blood per rectum
• 3) in 3rd or 4th portion of the duodenum near proximal suture line
• 4) treatment- bypass through noncontaminated field; resection of graft with aortic stump closure

• Anterior-
• 1- deep peroneal nerve (dorsiflexion, sensation between 1st and second toes)
• 2- anterior tibial artery

• Lateral-
• 1- superficial peroneal nerve (eversion, lateral foot sensation)

• Deep posterior-
• 1- tibial nerve (plantarflexion)
• 2- posterior tibial artery
• 3- peroneal artery

Superficial posterior- sural nerve

• 1- pallor
• 2- hair loss
• 3- dependent rubor
• 4- abnormal nail growth
• 5- slow capillary refill

most commonly due to atherosclerosis

statin drugs (lovastatin)

1) can increase risk of atherosclerosis

• Tx:
• 1- folate
• 2- B6
• 3- B12

• 1) medical therapy first:
• 1- ASA
• 2- smoking cessation
• 3- exercise until pain occurs to improve collaterals

- 2%/yr gangrene risk and 1%/yr amputation risk with claudication

Symptoms occur one level below occlusion:

1) Buttock claudication- aortoiliac disease

2) midthigh claudication- external iliac

3) calf claudication- common femoral artery or proximal superficial femoral artery disease

4) Foot claudication- distal superficial femoral artery or popliteal artery

lumbar stenosis

diabetic neuropathy

• 1) no femoral pulses
• 2) buttock or thigh claudication
• 3) impotence (from hypogastric obstruction and decreased flow in the internal iliacs)
• 4) lesion at aortic bifurcation or above

• - Hunter's canal (distal superficial femoral artery exits here).
• - Sartorious muscle covers hunter's canal

1) forms from abnormal pressure gradients

• 1- circumflex iliacs to subcostals
• 2- circumflex femoral arteries to gluteal arteries
• 3- geniculate arteries around the knee

• 1) budding from preexisting vessels
• 2) angiogenin involved

• 1) <0.9-start to get claudication (typically occurs at same distance each time)
• 2) <0.5- start to get rest pain (usually across the distal arch and foot)
• 3)<0.4- ulcers (usually starts in toes)
• 4) <0.3 gangrene

-ABIs can be very innaccurate in patients with diabetes secondary to incompressibility of vessels; often have to go off doppler waveforms in these patients

- In patients with claudication, the ABI in the extremity drops with walking (i.e. resting ABI may be 0.9 but can drop to <0.6 with exercise resulting in pain)

to find significant occlusion and at what level

If pulse volume recordings (PVRs) suggest significant disease- can also at times treat the patient with angiographic intervention; gold standard for vascular imaging

• 1- rest pain
• 2- ulceration or gangrene
• 3- lifestyle limitation
• 4- atheromatous embolization

• PTFE (gortex)- decreases patency when crosses knee
• Dacron- good for aorta and large vessels

• 1) most get aortobifemoral repair
• 2) in high-risk patients can perform bilateral axillary-femoral bypasses or an axillary-femoral bypass with a femoral-femoral crossover (keeps you out of the abdomen)

• 1) angioplasty with stent is 1st choice
• 2) if that fails can perform aortobifemoral repair or femoral to femoral crossover

• 1) 75% 5 year patency
• 2) improved patency rate in patients with surgery for claudication as opposed to limb salvage

• 1) 50% 5 year patency
• 2) patency not influenced by level of distal anastomosis
• 3) distal lesions more limb threatening because of lack of collaterals
• 4) bypasses distal to the knee, usually used only for limb salvage

synthetic grafts have decreased patency below the knee --> need to use saphenous vein

to avoid hostile conditions in the abdomen (aortic graft infections, multiple previous operations)

• 1- doubles blood flow to donor artery
• 2- can get vascular steal in donor leg

• 1) get lower extremity duplex to check for DVT
• 2) 2nd most common cause- edema from reperfusion injury

• 1) lactic acidosis
• 2) hyperkalemia
• 3) myoglobinuria
• 4) compartment syndrome

atherosclerosis

technical problem

amputation

• 1) noninfectious; can allow to autoamputate if just toes
• 2) larger lesions should probably be amputated
• 3) see if patient has correctible vascular lesion

• 1- infectious
• 2- amputation to remove infected necrotic material
• 3- antibiotics
• 4- surgical emergency

• 1) at metatarsal heads- 2nd MTP most common
• 2) diabetics; can have osteomyelitis
• 3) Tx:
• 1- nonweightbearing
• 2- debridement of metatarsal head (need to remove cartilage)
• 3- antibiotics
• 4- assess need for revascularization

• 1) excellent for common iliac lesions
• 2) best for short stenoses
• 3) intima usually ruptured and media stretched, pushes the plaque out
• 4) requires passage of wire first
• 5) pseudoaneurysm after arteriography- thrombin injection with ultrasound guidance
• - ultrasound duplex best 1st test for this

• 1) most likely to occur in the anterior compartment of leg (get footdrop)
• 2) pressure >20-30mmHg abnormal; consider fasciotomies --> leave open 5-10 days
• 3) Dx: based on clinical suspicion

• 1) most present with mild intermittent claudication
• 2) men, 40s; loss of pulses with plantarflexion
• 3) usually have medial deviation of artery around medial head of gastrocnemius muscle
• 4) treatment: resection of medial head of gastrocnemius muscle; may need arterial reconstruction

• 1) men, 40s; popliteal most common area
• 2) often bilateral -gangila originate from adjacent joint capsule or tendon sheath
• 3) Symptoms: intermittent claudication; changes in symptoms with knee flexion/extension
• 4) Diagnosis: angiogram
• 5) Treatment: vein graft if vessel occluded; otherwise just resection of cyst

• 1) internal iliac artery for children needing renal artery repair,
• 2) radial grafts for CABG
• 3) IMA for CABG

• 1) For:
• 1- gangrene
• 2- nonhealing ulcers
• 3- unrelenting rest pain not amenable to surgery

2) 50% mortality within 3 years of above-knee amputation (AKA) or below-knee amputation (BKA)

• 3) BKA- 80% heal, 70% walk again, 5% mortality
• 4) AKA- 90% heal, 30% walk again, 10% mortality

• 5) Emergency amputation for:
• 1- systemic complications
• 2- extensive infection
• 3- failure of antibiotics

• 1) usually do not have collaterals with emboli (do have collaterals with thrombosis)
• 2) usually do not have signs of chronic limb ischemia
• 3) contralateral leg usually has no chronic signs of ischemia and pulses are usually normal
• 4) usually have no history of claudication
• 1st pallor--> cyanosis--> marbling
• 5) symptoms: pain, pallor, pulselessness, paresthesia, poikilothermia, paralysis
• 6) Most common cause: atrial fibrillation
• 7) Other causes:
• 1- LV aneurysm with thrombus
• 2- prosthetic heart valve
• 3- cardiac tumors (myxoma)
• 4- paradoxical embolus from patent foramen ovale
• 5- peripheral arterial or aortic atherosclerotic plaque embolism
• 6- aortic or arterial aneurysm with embolism

• 8) common femoral artery most common site of peripheral obstruction from emboli
• 9) Treatment:
• 1- embolectomy usual; need to get pulses back; postop angiogram
• 2- consider fasciotomy if ischemia >4-6hrs --> permanent muscle and nerve damage begins at 4-6 hours
• 3- aortoiliac emboli (loss of pulses to both feet) can be treated with bilateral femoral artery cutdowns and bilateral embolectomies

• 1) renals most commonly involved; cholesterol clefts in small arteries
• 2) blue toe syndrome- flaking atherosclerotic emboli off abdominal aorta or branches
• 1- patients typically have good distal pulses
• 2- aortoiliac disease is most common source
• 3) Diagnosis:
• 1- need chest/abdomin/pelvis CT scan to look for aneurysmal source
• 2- Echo
• 3- angiogram to rule out atherosclerotic disease
• 4) Treatment-
• 1) may need aneurysm repair
• 2) endarterectomy
• 3) arterial exclusion with bypass

• Embolism:
• 1) arrythmia
• 2) no prior claudication or rest pain
• 3) normal contralateral pulses
• 4) no physical findings of chronic limb ischemia

• Thrombosis:
• 1) no arrhythmia
• 2) history of claudication or rest pain
• 3) contralateral pulses absent
• 4) physical findings of chronic limb ischemia

• 1) these patients usually do not have arrhythmias
• 2) do have a history of claudication and have signs of chronic limb ischemia and poor pulses in the contralateral leg
• 3) Treatment:
• 1- threatened limb- give heparin and go to OR for thrombectomy
• 2- limb not threatened- go to angiography for thrombolytics
• 3- thrombosis of PTFE graft- thrombolytics and anticoagulation; if limb threatened --> OR

• 1) right renal artery runs posterior to IVC
• 2) accessory renal arteries in 25%
• 3) most renal emboli from heart
• 4) renal atherosclerosis- left side, proximal 1/3, men
• Treatment: PTA with stent
• 5) fibromuscular dysplasia- right side, distal 1/3, women
• Treatment: PTA with stent
• 6) Suggestive of renovascular HTN:
• 1- bruits
• 2- diastolic BP >115
• 3- worsening HTN
• 4- children
• 5- premenopausal women
• 6- rapid onset after age 50
• 7- HTN resistant to drug therapy

• 7) need to rule out other sources of HTN (pheochromocytoma, etc)
• 8) Diagnosis of renal artery stenosis: angiogram
• 9) Treatment: PTA with stent
• 10) Indications for nephrectomy with renal HTN:
• 1- atrophic kidney <6cm
• 2- minimal collaterals with persistently high renin levels

• 1) proximal lesions usually asymptomatic secondary to increased collaterals
• 2) subclavian most common site of stenosis
• 3) Treatment:
• 1- PTA w/stent
• 2- can also perform common carotid to subclavian bypass

• 1) proximal subclavian artery stenosis resulting in reversal of flow through ipsilateral vertebral artery into subclavian
• 2) operate with limb or neurologic (usually vertebrobasilar) symptoms
• 3) Treatment:
• 1- PTA
• 2- carotic to subclavian bypass

1) subclavian vein- passes over the 1st rib anterior to the anterior scalene muscle, then behind clavicle

2) brachial plexus and subclavian artery- pass over the 1st rib posterior to the anterior scalene muscle, and anterior to the middle scalene muscle

3) Diagnosis- CXR, c-spine x-ray, angiography if thought to be vascular etiology, EMG

4) can get back and neck symptoms

4) Adson's test- decreased radial pulse with head turned ipsilateral side (subclavian artery compression)

5) Tinsel's test- tapping reproduces symptoms

6) neurologic involvement- much more common than vascular

7) #1 anatomic abnormality- cervical rib

8) #1 cause of pain- brachial plexus irritation

• 1) usually have normal neurologic exam
• 2) increased back + neck symptoms
• 3) palpation/manipulation- can increase symptoms
• 4) ulnar nerve distribution (C8-T1) most common
• 5) triceps weakness/atrophy, weakness of intrinsic muscle of hand, weak wrist flexion (located on inferior portion of brachial plexus)
• 7) radial nerve- located on superior portion of brachial plexus (finger extensors, wrist extension)
• 8) Treatment:
• 1- resection of cervical ribs
• 2- divide anterior scalenes and middle scalenes +/- 1st rib

• 1) compression usually secondary to anterior scalene hypertrophy (pitchers)
• 2) absent radial pulse with maximal arm abduction
• 3) Treatment:
• Surgery :
• 1-cervical rib and 1st rib resection
• 2- divide anterior scalene muscle
• 3- bypass graft

• 1) usually presents as effort-induced thrombosis of subclavian vein (paget-von schrotter disease)
• 2) venous thrombosis- much more common than arterial
• 3) venography- gold standard for diagnosis
• 4) male gender; pain and swelling increased with activity, decreased with rest
• 5) 80% have associated thoracic outlet problem
• 6) Treatment:
• 1- thrombolytics, heparin, warfarin initial treatment
• 2- repair at that admission

• 1) motor function can remain in digits after prolonged ischemia because motor groups are in proximal forearm
• 2) see chart on page 194 on workup for patients with hand ischemia

1) overal mortality 50-70%

• 2) findings on abdominal CT that suggest intestinal ischemia-
• 1- bowel wall thickening
• 2- intramural gas
• 3- portal venous gas
• 4- vascular occlusion

• 3) Most common causes of visceral ischemia:
• 1- acute embolic occlusion- 50%
• 2- thrombotic occlusion- 25%
• 3- low flow state- 15%
• 4- venous thrombosis- 5%

1) most commonly occurs near origin of SMA- heart #1 source

2) pain out of proportion to exam; pain usually of sudden onset; hematochezia; peritoneal signs late finding

• 3) May have history of:
• 1- atrial fibrillation
• 2- endocarditis
• 3- recent MI
• 4- recent angiography

4) Diagnosis: angiogram or abdominal CT with IV contrast

• 5) Treatment:
• 1- volume resuscitation
• 2- antibiotics
• 3- embolectomy
• 4- resect infarcted bowel
• 5- heparin

• 1) usually have history of chronic problems (food fear from mesenteric angina)
• 2) may have a history of vasculitis or hypercoagulable state
• 3) symptoms: similar to embolism; may have developed some collaterals
• 4) Diagnosis: angiogram or abdominal CT with IV contrast
• 5) Treatment:
• 1- thrombectomy
• 2- usually need SMA bypass
• 3- resection of infarcted bowel
• 4- heparin

• 1) usually short segments of intestine involved; bloody diarrhea, crampy abdominal pain
• 2) may have a history of vasculitis, hypercoagulable state, portal HTN
• 3) Diagnosis: abdominal CT scan or angiogram
• 4) Treatment: heparin, thrombolytics; can try mesenteric vein thrombectomy is diagnosed early; resection of infarcted bowel

1) spasm, low-flow states, hypovolemia, hemoconcentration, digoxin --> final common pathway is low cardiac output state to visceral vessels

• 2) risk factors:
• 1- prolonged shock
• 2- CHF
• 3- prolonged cardiopulmonary bypass

3) bloody diarrhea, pain

4) watershed areas (Griffith's and Sudak's points) most vulnerable

• 5) Treatment:
• 1- volume resuscitation
• 2- glucagon
• 3- papaverine
• 4- nitrates can increase visceral blood flow
• also need to increase cardiac output; resection of infarcted bowel

• 1) causes celiac compression
• 2) bruit near epigastrium, chronic pain, weight loss, diarrhea
• 3) Treatment: transect median arcuate ligament, may need arterial reconstruction

• 1) weight loss secondary to food fear
• 2) visceral angina occus 30 minutes after meals (food fear)
• 3) may need PTA, bypass, or endarterectomy
• 4) get lateral visceral vessel aortography to see origins of celiac and SMA

is an important collateral between the SMA and IMA

rupture

thrombosis and emboli

1) Repair all spanchnic aneurysms when diagnosed (50% risk for rupture) except splenic

2) splenic artery aneurysm- most common visceral aneurysm (more common in women, 2% risk of rupture)

• 3) Repair splenic artery aneurysms if:
• 1-symptomatic
• 2- patient is pregnant
• 3- occurs in women of childbearing age

4) High rate of pregnancy-related rupture- usually occurs in 3rd trimester

5) diameters >2cm considered aneurysmal

6) most visceral aneurysms are treated with exclusion and bypass graft

7) splenic and proximal common hepatic can just be excluded (have good collaterals)

• 8) risk factors:
• 1- medial fibrodysplasia
• 2- portal HTN
• 3- arterial disruption secondary to inflammatory disease (i.e. pancreatitis)

• 1) surgical indications:
• 1- symptomatic (thrombosis, emboli, or compression)
• 2- >3cm
• 3- mycotic

2) bypass with exclusion

• 1) Surgical indications:
• 1- symptomatic (thrombosis, emboli, or compression)
• 2- >2.5 cm
• 3- mycotic

2) Treatment: bypass with exclusion

• 1) most common peripheral aneurysm
• 2) leg exam reveals prominent popliteal pulses
• 3) 1/2 are bilateral
• 4) 1/2 have another aneurysm elsewhere (AAA, femoral etc)
• 5) most likely to get thrombosis or emboli with limb ischemia
• 6) can also get leg pain from compression of adjacent structures
• 7) Surgical indicaitons:
• 1- symptomatic
• 2- >2cm
• 3- mycotic
• 8) Diagnosis: ultrasound
• 9) Treatment: exclusion and bypass of all popliteal aneurysms; 25% have complication that requires amputation if not treated

• 1) collection of blood in continuity with the arterial system but unenclosed by all 3 layers of the arterial wall
• 2) can result from disruption of a suture line between graft and artery or from percutaneous interventions
• 3) Treatment: if occurs after percutaneous intervention, need ultrasound-guided compression with thrombin injection --> if flow remains in the pseudoaneurysm or if pseudoaneurysm is at a suture site, need surgical repair

• 1) Surgical indications:
• 1- symptomatic
• 2- expansion
• 3- >1.5cm
• 4- women who want pregnancy

• 2) Treatment-
• 1- reconstruction with vein patch
• 2- nephrectomy if rupture occurs

may be an option for many of the aneurysms discussed previously

• 1) young women; HTN if renal involved
• 2) renal (right side) most commonly involved vessel, followed by carotid and iliac
• 2) string of beads
• 3) medial fibrodysplasia most common variant (80-90%)
• 4) Treatment:
• 1- PTA (1st choice)
• 2- bypass

• 1) young men, smokers, corkscrew collateral on angiogram and severe distal disease
• 2) severe rest pain with bilateral ulceration
• 3) gangrene of the digits, especially the fingers
• 4) normal arterial tree proximal to popliteal and brachial vessels (small vessel disease)
• 5) Treatment: stop smoking or will require continued amputations

• Marfan's disease
• 1) type 1 collagen defect
• 2) marfanoid habitus
• 3) retinal detachment
• 4) aortic root dilatation

• Ehlers-Danlos syndrome
• 1) many type of collagen defects identified

• 2)
• - easy bruising
• - hypermobile joints
• - tendency for arterial rupture, especially abdominal vessels
• - get aneurysms and dissections

3) no angiograms --> risk of laceration to vessel

4) often too difficult to repair and need ligation of vessels to control hemorrhage