Flashcards in Chapter 27: Vascular Deck (394):
Most common congenital hyper coagulable disorder
Resistance to activated protein C (Leiden factor)
Most common acquired hyper coagulable disorder
1) Foam cells (macrophages have absorbed fat and lipids in the vessel wall)
2) Smooth muscle cell proliferation (caused by growth factors released from macrophages; results in wall injury)
3) Intimal disruption (from smooth muscle cell proliferation)
What stage of athersclerosis causes thrombus formation?
Third - intimal disruption: leads to exposure of collagen in vessel wall and eventual thrombus formation -> fibrous plaques then form in these areas with underlying atheromas
Risk factors for atherosclerosis
Smoking, HTN, hypercholesterolemia, DM, hereditary factors
3rd most common cause of death in the United States
Most important risk factor for stroke
Supple 85% of blood supply to the brain
Most common site of stenosis in cerebrovascular disease
Type of flow from normal internal carotid artery
Continuous forward flow
1st branch off the internal carotid artery
Type of flow from external carotid artery
1st branch of the external carotid artery
Superior thyroid artery
Communication between the ICA and ECA
Ophthalmic artery (off ICA) and internal maxillary artery (off ECA)
Most commonly diseased intracranial artery
Middle cerebral artery
Most commonly from arterial embolization from the ICA (not thrombosis)
- Can also occur from a low-flow state through a severely stenotic lesion
Cerebral ischemic events
2nd most common source of cerebral emboli
Lesion: mental status changes, release, slowing
Anterior cerebral artery events
Lesion: contralateral motor and speech (if dominant side); contralateral facial droop
Middle cerebral artery events
Lesion: vertigo, tinnitus, drop attacks, incoordination
Posterior cerebral artery events
Occlusion of the ophthalmic branch of the ICA (visual changes -> shade coming down over eyes); visual changes are transient
What do you see on ophthalmologic exam in amaurosis fugax?
Treatment: carotid traumatic injury with major fixed deficit:
- If occluded, do not repair -> can exacerbate injury with bleeding
- If not occluded -> repair with carotid stent or open procedure
Indications for CEA
Symptomatic > 70%, asymptomatic > 80%
When do you consider CEA in a recent completed stroke?
Wait 4-6 weeks and then perform CEA if it meets criteria (bleeding risk if performed earlier)
Indications for emergenct CEA
May be of benefit with fluctuating neurologic symptoms or crescendo / evolving TIAs
When do you use a shunt during CEA?
Use a shunt during CEA from stump pressures > 50 or if contralateral side is tight
What side do you repair in bilateral stenosis during CEA?
Repair the tightest side first if the patient has bilateral stenosis
What side do you repair if the patient has equally tight carotid stenosis bilaterally during CEA?
Repair the dominant side first if the patient has equally tight carotid stenosis bilaterally
Complications from repair during CEA
- Vagus nerve injury
- Hypoglossal nerve injury
- Glossopharyngeal nerve injury
- Ansa cervicalis
- Mandibular branch of facial nerve
Most common cranial nerve injury with CEA
Vagus nerve: secondary to vascular clamping during endarterectomy; patients get hoarseness (recurrent laryngeal nerve comes off vagus)
CEA complication: tongue deviates to the side of injury-> speech and mastication difficulty
Hypoglossal nerve injury
CEA complication: rare, occurs with really high carotid dissection -> causes difficulty swallowing
Glossopharyngeal nerve injury
CEA complication: innervation to strap muscles; no serious deficits
CEA complication: affects corner of mouth (smile)
Mandibular branch of facial nerve
Treatment: acute event immediately after CEA
Back to OR to check for flap or thrombosis
Pulsatile, bleeding mass after CEA
Tx: drape and prep before intubation, intubate, then repair
Why do 20% have hypertension following CEA?
Caused by injury to the carotid body
Tx: HTN following CEA
Nipride to avoid bleeding
Most common cause of non-stroke morbidity and mortality following CEA
Restonosis rate after CEA
Indications for carotid stenting
For high-risk patients (e.g. patients with previous CEA and restenosis, multiple medical comorbidities, previous neck XRT)
Pathway of the vertebrobasilar artery
Two vertebral arteries arise from the subclavian arteries and combine to form a single basilar artery; the basilar then splits into two posterior cerebral arteries
When do you see symptoms in vertebrobasilar artery disease?
Usually need basilar artery or bilateral vertebral artery disease to have symptoms
Tx: vertebrobasilar artery disease
PTA with stent
What causes vertebrobasilar artery disease?
Caused by atherosclerosis, spurs, band; get vertebrobasilar insufficiency
Symptoms: diplopia, vertigo, tinnitus, drop attacks, incoordination
Vertebrobasilar artery disease
Tx: vertebrobasilar artery disease
PTA with stent
Present as a painless neck mass, usually near bifurcation, neural crest cells; are extremely vascular
Carotid body tumors
What are the aortic arch vessels?
Innominate artery (which branches into the right subclavian and right common carotid arteries), the left common carotid artery, and the left subclavian artery
- Often asymptotic and picked up on routine CXR
- Can get compression of vertebra (back pain), RLN (voice changes), bronchi (dyspnea or PNA), or esophagus (dysphagia)
Ascending aortic aneurysm
Indications for repair in ascending aortic aneurysm
Acutely symptomatic, > 5.5 cm (with Marfan's > 5.0cm), or rapid increase in size ( > 0.5 cm/yr)
Indications for repair of descending aortic aneurysm (also thoracoabdominal aneurysms)
If endovascular repair possible > 5.5 cm.
If open repair needed > 6.5cm
Risk of mortality or paraplegia endovascular repair vs open repair
Less with endovascular repair (2-3%) compared to open repair (20%)
How can you help prevent paraplegia with open repair?
Reimplant intercostal arteries below T8 to help prevent paraplegia with open repair
Classifications of Aortic Dissection
What is the difference between the Stanford classification and the DeBakey Classification?
- Stanford: based on presence or absence of involvement of ascending aorta
- DeBakey: based on the site of tear and extent of dissection
Stanford classification: Class A
any ascending aortic involvement
Stanford classification: class B
Descending aortic involvement only
Type I DeBakey
Ascending and descending
Type II DeBakey
Type III DeBakey
Where do most dissections start?
In the ascending aorta
What can aortic dissection mimic?
Symptoms: tearing like chest pain, can have unequal pulses (or BP) in upper extremities
What is present in 95% of patients with aortic dissection?
95% of patients have severe HTN at presentation
Risk factors for aortic dissection
Marfan's syndrome, previous aneurysm, atherosclerosis
Dx: aortic dissection
Chest CT with contrast
Where does aortic dissection occur?
Dissection occurs in the medial layer of blood vessel wall
Incidence of aortic insufficiency in aortic dissection
Aortic insufficiency: occurs in 70%, caused by annular dilatation or when aortic valve cusp is sheared off
What arteries are at risk in aortic dissection?
Can also have occlusion of the coronary arteries and major aortic branches
What is usually the cause of death in aortic dissection?
Death with ascending aortic dissections usually secondary to cardiac failure form aortic insufficiency, cardiac tamponade or rupture
Medical treatment initially for aortic dissections
Control BP with IV beta-blockers (e.g. esmolol) and Nipride
When to operate on ascending aortic dissections?
Operate on all ascending aortic dissections.
- Tx: need open repair; graft is placed to eliminate flow to the false lumen
When to operate on descending aortic dissections?
Only operate on descending aortic dissections with visceral or extremity ischemia or if contained rupture
- Tx: Endograft or open repair; can also just place fenestrations in the dissection flap to restore blood flow to viscera or extremity if ischemia is the problem.
Follow up for surgery for aortic dissection
Follow these patients with lifetime serial scans (MRI to decrease radiation exposure)
Why do people status post aortic dissection repair need lifetime follow up?
30% eventually get aneurysm formation requiring surgery
Post op complications for thoracic aortic surgery
MI, renal failure, paraplegia (descending thoracic aortic surgery)
Why is paraplegia a risk in aortic dissection repair?
Paraplegia is caused by spinal cord ischemia due to occlusion of intercostal arteries and artery of Adamkiewicz that occurs with descending thoracic aortic surgery
Normal aorta size
What causes AAA?
Results from degeneration of the medial layer
Risk factors for AAA
males, age, smoking, family history
How do AAA usually present?
- Usually found incidentally.
- Can present with rupture, distal embolization, or compression of adjacent organs
Leading cause of death in AAA
Rupture: leading cause of death without an operation
Symptoms: back or abdominal pain, can have profound hypotension
Dx: Ruptured AAA
Ultrasound or abdominal CT
CT findings in ruptured AAA
CT shows fluid in the retroperitoneal space and extraluminal contrast with rupture
Where is AAA most likely to rupture?
Most likely to rupture on left posterolateral wall, 2-4 cm below renals
When is AAA more likely to rupture?
More likely to rupture in the presence of diastolic HTN or COPD (thought to be predictors of expansion)
Rate of mortality with rupture of AAA if patient reaches hospital alive
50% mortality rate with rupture if patient reaches hospital alive
Indications for surgical repair of AAA
Repair if symptomatic, > 5.5 cm, or growth > 0.5 cm/yr
When do you reimplant the inferior mesenteric artery in surgical repair of ruptured AAA?
Reimplant IMA if back pressures
What arteries need ligation in ruptured AAA repair?
Ligate bleeding lumbar arteries
What artery needs ensured flow in aorto-bifemoral repair instead of straight tube graft in ruptured AAA repair?
If performing an aorto-bifemoral repair: ensure flow to at least one internal iliac artery (hypogastric artery) to avoid vasculogenic impotence
Graft used for repair of AAAs
Usually use a straight tube Dacron graft for repair of AAAs
Complications of AAA repair
Major vein injury with proximal cross-clamp. Impotence. MI. Renal failure. Graft infection. Pseudo aneurysm. Atherosclerotic occlusion. Diarrhea.
AAA complication: major vein injury with proximal cross-clamp
Retro-aortic left renal vein
AAA complication: impotence
In 1/3 secondary to disruption of autonomic nerves and blood flow to the pelvis
Rate of mortality with elective AAA repair
5% mortality with elective repair
#1 cause of acute death after surgery
#1 cause of late death after surgery
Risk factors for mortality in AAA repair
Creatinine > 1.8 (#1), CHF, EKG ischemia, pulmonary dysfunction, older age, females
#1 risk factor for mortality after AAA repair
Creatinine > 1.8
Graft infection rate s/p AAA repair
Pseudoaneurysm formation s/p graft placement for AAA repair
Most common later complication after aortic graft placement
What is diarrhea (especially bloody) worrisome for after AAA repair?
Why is ischemic colitis a possible complication in AAA repair?
Inferior mesenteric artery is often sacrificed with AAA repair and can cause ischemia (most commonly left colon)
Dx: ischemic colitis s/p AAA repair
Endoscopy or abdominal CT: middle and distal rectum are spared from ischemia (middle and inferior rectal arteries are branches off the internal iliac artery)
When do you go to OR for ischemic colitis s/p AAA repair?
If patient has peritoneal signs, mucosa is black on endoscopy, or part of the colon looks dead on CT scan -> take to OR for colectomy and colostomy placement
AAA: ideal criteria for endovascular repair:
- Neck length
- Neck diameter
- Neck angulation
- Common iliac artery length
- Common iliac artery diameter
- Neck length: > 15mm
- Neck diameter: 20-30mm
- Neck angulation: 10mm
- Common iliac artery diameter: 8-18mm
- Other: non-tortuous, noncalcified iliac arteries, lack of neck thrombus
AAA repair: failure site -> Type 1 endoleak
Proximal or distal graft attachment sites
Tx: extension cuffs
AAA repair: failure site -> Type 2 endoleak
Collaterals (eg patent lumbar, IMA, intercostals, accessory renal)
Tx: observe most, percutaneous coil embolization if pressurizing aneurysm
AAA repair: failure site -> Type 3 endoleak
Overlap sites when using multiple grafts or fabric tear
Tx: Secondary endograft to cover overlap site or tear
AAA repair: failure site -> Type 4 endoleak
Graft wall porosity or suture holes
Tx: Observe, can place nonporous stent if that fails
AAA repair: failure site -> Type 5 endoleak (endotension)
Expansion of aneurysm without evidence of leak
Tx: repeat EVAR or open repair
- Occurs in 10% of patients with AAA; males
- Weight loss, increased ESR, thickened rim above calcifications on CT scan
- Not secondary to infection: just an inflammatory process
Anatomical problems to consider in inflammatory aneurysms
- Can get adhesions to the 3rd and 4th portion of the duodenum
- Ureteral entrapment in 25%
How do you prevent ureteral injury (25%) in repair of inflammatory aneurysms?
May need to place preoperative ureteral stents to help avoid injury.
Treatment: inflammatory aneurysm
Inflammatory process resolves after aortic graft placement
Cause of mycotic aneurysms
How do bacteria cause mycotic aneurysms?
Bacteria infect atherosclerotic plaque, cause aneurysm
- Pain, fevers, positive blood cultures in 50%
- Periaortic fluid, gas, retroperitoneal soft tissue edema, lymphadenopathy
Treatment: mycotic aneurysms
Usually need extra-anatomic bypass (axillary-femoral with femoral-to-femoral crossover) and resection of infrarenal abdominal aorta to clear infection
Causes of aortic graft infections
#2 E. coli
- Cause: 1) Staph 2) Ecoli
- See fluid, gas, thickening around graft
- Blood cultures negative in many patients
Aortic graft infections
What are aortic graft infections most common in?
More common with grafts going to the groin (e.g., aorto-bifemoral grafts)
Treatment: aortic graft infections
Bypass thru non-contaminated field (e.g. axillary-femoral bypass with femoral-to-femoral crossover) and then resect the infected graft
- Usually occurs > 6 months after abdominal aortic surgery
- Herald bleed with hematemesis, then blood per rectum
Where does the graft erode in aortoenteric fistula?
Graft erodes into 3rd or 4th portion of duodenum near proximal suture line
Treatment: aortoenteric fistula
Bypass through non-contaminated field (e.g. axillary-femoral bypass with femoral-to-femoral crossover), resect graft, and then close hole in the duodenum
Standard treatment for an infected aortic valvular prosthesis
An axillobifemoral bypass is performed first. This is followed a few days later by removal of the infected aortic prosthesis and careful oversewing of the aortic stump as illustrated
Components of leg compartments
Anterior: deep peroneal nerve (dorsiflexion, sensation between 1st and 2nd toes), anterior tibial artery
- Lateral: superficial peroneal nerve (eversion, lateral foot sensation)
- Deep posterior: tibial nerve (plantar flexion), posterior tibial artery, peroneal artery
- Superficial posterior: sural nerve
Components of anterior leg compartment
Deep peroneal nerve (dorsiflexion, sensation between 1st and 2nd toes), anterior tibial artery
Components of lateral leg compartment
Superficial peroneal nerve (eversion, lateral foot sensation)
Components of deep posterior leg compartment
Tibial nerve (plantar flexion), posterior tibial artery, peroneal artery
Components of superficial posterior leg compartment
Signs of PAD
Pallor, dependent rubor, hair loss, slow capillary refill
#1 preventative agent for atherosclerosis
Statin drugs (lovastatin)
Can increase risk of atherosclerosis.
- Tx: folate and B12
Treatment of claudication
Medical therapy first: ASA, smoking cessation, exercise until pain occurs to improve collaterals
Level of occlusion: buttock claudication
Level of occlusion: mid-thigh claudication
Level of occlusion: calf claudication
Common femoral artery or proximal superficial femoral artery disease
Level of occlusion: foot claudication
Distal superficial artery or popliteal disease
How can you remember the symptoms associated with the level of occlusion in PAD?
Symptoms occur one level below occlusion
What can mimic claudication?
What can mimic rest pain in PAD?
- No femoral pulses
- Buttock or thigh claudication
- Impotence (from decreased flow in the internal iliacs)
Where is the lesion in Leriche syndrome?
Lesion at aortic bifurcation or above
Treatment: Leriche syndrome
Aorto-bifemoral bypass graft
Most common atherosclerotic occlusion in the lower extremities
Hunter's canal (distal superficial femoral artery exits here)
What muscle covers Hunter's canal?
What forms collateral circulation?
Forms form abnormal pressure gradients
Collateral circulation of circumflex iliacs
Circumflex iliacs to subcostals
Collateral circulation of circumflex femoral arteries
Circumflex femoral arteries to gluteal arteries
Collateral circulation around the knee
Budding from preexisting vessels; angiogenin involved
Start to get claudication (typically occurs at same distance each time)
Start to get rest pain (usually across the distal arch and foot)
Ulcers (Usually starts in toes)
Why can ABIs be very inaccurate in patients with diabetes?
Secondary to incompressibility of vessels; often have to go off Doppler waveforms in these patients
How does walking affect the ABI?
In patients with claudication, the ABI in the extremity drops with walking (i.e. resting ABI may be 0.9 but can drop to
Used to find significant occlusion and at what level
Pulse volume recordings (PVRs)
When is arteriogram indicated in PAD?
If PVRs suggest significant disease - can also at times treat the patient with percutaneous intervention; gold standard for vascular imaging.
Gold standard for vascular imaging
Surgical indications for PAD
Rest pain, ulceration or gangrene, lifestyle limitation, atheromatous embolization
Only for bypasses above the knee; need to use vein for below the knee bypasses
Good for aorta and large vessels
Most get aorto-bifemoral repair
Aortoiliac occlusive disease
How do you prevent vasculogenic impotence and pelvic ischemia during repair of aortoiliac occlusive disease?
Need to ensure flow to at least 1 internal iliac artery (hypogastric artery; want to see good back-bleeding from at least 1 of the arteries, otherwise need a bypass to an internal iliac artery) when performing aorto-bifemoral repair
Treatment for isolated iliac lesions
PTA with stent 1st choice; if that fails, consider femoral-to-femoral crossover
- 75% 5-year potency
- improved patency with surgery for claudication as opposed to limb salvage
Popliteal artery exposure below the knee:
- Posterior muscle
- Anterior muscle
Posterior muscle: gastrocnemius
Anterior muscle: popliteus
Arteries useful in femoral-distal grafts
Peroneal, anterior tibial, or posterior tibial artery
Rate of potency of femoral-distal grafts
50% 5-year potency; potency not influenced by level of distal anastomosis
Why are distal lesions more limb threatening?
Because of lack of collaterals
When are bypasses to distal vessels usually performed?
Usually used only for limb salvage
If you are going to perform distal bypass on the leg, what do you need to ensure?
Bypassed vessel needs to have run-off below the ankle for this to be successful
Why use saphenous vein for bypass below the knee?
Synethetic grafts have decreased patency below the knee -> need to use saphenous vein.
When to consider extra-anatomic grafts?
Can be used to avoid hostile conditions in the abdomen (multiple previous operations in a frail patients_
Doubles blood flow to donor artery; can get vascular steal in donor leg
Femoral-to-femoral crossover graft
Dx: early swelling following lower extremity bypass
Reperfusion injury and compartment syndrome
Dx: late swelling following lower extremity bypass
Tx: heparin, coumadin
Complications of reperfusion of ischemic tissue
Compartment syndrome, lactic acidosis, hyperkalemia, myoglobinuria
#1 cause of early failure of reversed saphenous vein grafts
#1 cause of late failure of reversed saphenous vein grafts
Noninfectious, can allow to autoamputate if small or just toes.
Management of dry gangrene
- Large lesions should be amputated
- See if patient has a correctable vascular lesion
Infectious, need to remove infected necrotic material ; antibiotics
When is wet gangrene considered a surgical emergency?
If extensive infection (Eg swollen red toe with pus coming out and red streaks up leg) or systemic complication occur (e.g. septic) -> may need emergency amputation
- At metatarsal heads
- Diabetics, can have osteomyelitis
Mal perforans ulcer
MC'ly involved joint in mal performs ulcer
2nd MTP joint most common
Tx: mal perforans ulcer
Non-weightbearing, debridement of metatarsal head (need to remove cartilage), antibiotics; assess need for revascularization
- Excellent for common iliac artery stenosis
- Best for short stenoses
Percutaneous transluminal angioplasty (PTA)
How does percutaneous transluminal angioplasty (PTA) work?
Intimal usually ruptured and media stretched, pushes the plaque out.
- Requires passage of wire first.
What causes compartment syndrome?
Is caused by repercussion injury to the extremity (mediated by PMNs; occurs with cessation of blood flow to extremity and repercussion > 4-6 hours later).
What causes increased compartment pressures in compartment syndrome?
Reperfusion injury leads to swelling of the muscle compartments -> raising compartment pressures, which can lead to ischemia
Symptoms of compartment syndrome
Pain with passive motion; extremity feels tight and swollen
Where is compartment syndrome most likely to occur?
Most likely to occur in the anterior compartment of leg (get foot drop)
Dx / Tx: compartment syndrome
Dx: often based on clinical suspicion; compartment pressure > 20 - 30 mmHg abnormal
Tx: fasciotomies (get all 4 compartments if in lower leg) -> leave open 5-10 days
- Most present with mild intermittent claudication
- Men, 40s, loss of pulses with plantar flexion
Popliteal entrapment syndrome
What leads to popliteal entrapment syndrome?
Have medial deviation of artery around medial head of gastrocnemius muscle
Tx: popliteal entrapment syndrome
Resection of medial head of gastrocnemius muscle; may need arterial reconstruction
- Men, 40s, popliteral fossa most common area
- Symptoms: intermittent claudication, changes in symptoms with knee flexion / extension
Adventitial cystic disease
Why is adventitial cystic disease most often bilateral?
Ganglia originate from adjacent joint capsule or tendon sheath
Dx / Tx: adventitial cystic disease
Tx: resection of cyst; vein graft if the vessel is occluded
What are arterial autografts?
Radial artery grafts for CABG, IMA from CABG
When do you amputate?
For gangrene, large non-healing ulcers or unrelenting rest pain not amenable to surgery.
Rate of mortality within 3 years for leg amputation
- ___% heal
- ___% walk again
- ___% mortality
70% walk again
- ___% heal
- ___% walk again
- ___% mortality
30% walk again
Indications for emergency amputation
Systemic complications or extensive infection
Embolism or Thrombosis?
- No prior claudication or rest pain
- Normal contralateral pulses
- No physical findings of chronic limb ischemia
Embolism or thrombosis?
- No arrhythmia
- History of claudication or rest pain
- Contralateral pulses absent
- Physical findings of chronic limb ischemia
- Usually do not have collaterals, signs of chronic limb ischemia, or history of claudication with emboli (do have collaterals with thrombosis)
Acute arterial emboli
Contralateral leg in acute arterial emboli
Contralateral leg usually has no chronic signs of ischemia and pulses are usually normal
Symptoms: pain, paresthesia, poikilothermia, paralysis
Acute arterial emboli
Extremity ischemia evolution in acute arterial emboli
Pallor (white) -> cyanosis (blue) -> marbling
MCC acute arterial emboli
Common causes of acute arterial emboli
A fib (MCC), recent MI with LV thrombus, myxoma, aorto-iliac disease
MC site of peripheral obstruction from emboli
Common femoral artery
Tx: acute arterial emboli
Embolectomy usual; need to get pulses back; post op angiogram
- Consider fasciotomy is ischemia > 4-6 hours
When do you consider fasciotomy in acute arterial emboli?
If ischemia > 4-6 hours
Treatment possibility in aortoiliac emboli (loss of both femoral pulses)
Can be treated with bilateral femoral artery cutdown and bilateral embolectomies
Cholesterol clefts that can lodge in small arteries
Most common site of atheroma embolization
Flaking atherosclerotic emboli off abdominal aorta or branches
- Patients typically have good distal pules
Blue toe syndrome
MC source of blue toe syndrome
Dx: atheroma embolism
Chest/abdomen/pelvis CT scan (look for aneurysmal source) and ECHO (clot or myxoma in heart)
Tx: atheroma embolism
May need aneurysm repair or arterial exclusion with bypass
Do patients with acute arterial thrombosis usually have arrhythmia?
No. These patients usually do not have arrhythmias.
What is the usually history in acute arterial thrombosis?
Do have a history of claudication and have signs of chronic limb ischemia and poor pulses in the contralateral leg.
Tx: acute arterial thrombosis
Threatened limb (loss of sensation or motor function) -> give heparin and go to OR for thrombectomy
If limb is not threatened: angiography for thrombolytics
Treatment: thrombosis of PTFE graft
Thrombolytics and anticoagulation; if limb threatened -> OR for thrombectomy
Where does the right renal artery run?
Posterior to IVC
Rate of accessory renal arteries in humans
Accessory renal arteries in 25%
Bruits. Diastolic blood pressure > 115, HTN, in children or premenopausal women, HTN resistant to drug therapy.
Renovascular HTN (renal artery stenosis)
- Left side
- Proximal 1/3
- Right side
- Distal 1/3
Dx: renovascular HTN (renal atherosclerosis, fibromuscular dysplasia)
Tx: renovascular HTN (renal atherosclerosis, fibromuscular dysplasia)
PTA (percutaneous transluminal angioplasty); place stent if due to atherosclerotic disease
Indications for nephrectomy with renal HTN
Occlusive disease in the upper extremity: why are proximal lesions usually asymptomatic?
Secondary to increased collaterals
Most common site of upper extremity stenosis
Tx: occlusive disease of the upper extremity
PTA with stent; common carotid to subclavian artery bypass if that fails.
Proximal subclavian artery stenosis resulting in reversal of flow through ipsilateral vertebral artery into the subclavian artery
Subclavian steal syndrome
When do you operate in subclavian steal syndrome?
Operate with limb or neurologic symptoms (usually vertebrabasilar symptoms)
Tx: subclavian steal syndrome
PTA with stent to subclavian artery, common carotid to subclavian artery bypass if that fails.
Passes over the first rib anterior to the anterior scalene muscle, then behind clavicle
Passes over the first rib posterior to the anterior scalene muscle and anterior to the middle scalene muscle
Brachial plexus and subclavian artery
General symptoms: back, neck, and/or arm pain / weakness / tingling (often worse with palpation / manipulation)
Thoracic outlet syndrome
Dx: thoracic outlet syndrome
Cervical spine and chest MRI, duplex US (vascular etiology), electromyelogram (EMG; neurologic etiology)
If neurologic or vascular involvement more common in thoracic outlet syndrome?
Neurologic involvement - much more common than vascular
#1 anatomic abnormality in thoracic outlet syndrome
#1 cause of pain in thoracic outlet syndrome
Brachial plexus irritation
How does the exam look in thoracic outlet syndrome?
Usually have normal neurologic exam; tapping can reproduce symptoms (Tinsel's test)
Most common nerve distribution causing pain in thoracic outlet syndrome
Ulnar nerve distribution (C8-T1) - inferior portion of brachial plexus
Symptoms of ulnar nerve distribution involvement in thoracic outlet syndrome
Tricep muscle weakness and atrophy, weakness of intrinsic muscles of hand, weak wrist flexion.
Tx: thoracic outlet syndrome
Cervical rib and 1st rib resection, divide anterior scalene muscle
Usually presents as effort-induced thrombosis of subclavian vein (Paget-von Schrotter disease; baseball pitchers) - acutely painful, swollen, blue limb
Subclavian vein TOS
What type of thrombosis is involved in subclavian vein TOS
Venous thrombosis is much more common than arterial
Dx: subclavian vein causing TOS
Venography is the gold standard for diagnosis, but duplex US makes the diagnosis and is quicker to get.
Rate of thoracic outlet problem in subclavian vein problem causing TOS
80% have associated thoracic outlet problem.
Tx: subclavian vein TOS
Thrombolytics initially; repair at that admission (Cervical rib and 1st rib resection, divide anterior scalene)
Least common cause of TOS
What is the cause of subclavian artery involvement in TOS?
Compression usually secondary to anterior scalene hypertrophy (weight lifters)
Symptoms: subclavian artery TOS
Hand pain from ischemia
Test used to confirm subclavian artery TOS
Adson's test: absent radial pulse with head turned to ipsilateral side
Dx / Tx: subclavian artery TOS
Dx: duplex US or angiogram (gold standard)
Tx: surgery -> cervical rib and 1st rib resection, divide anterior scalene muscle; possible bypass graft if artery is too damaged or aneursymal
Why can motor function be preserved in digits after prolonged hand ischemia?
Motor function can remain in digits after prolonged hand ischemia because motor groups are in the proximal forearm.
- Overall mortality 60%
- Usually involve SMA
- CT findings: vascular occlusion, bowel wall thickening, intramural gas, portal venous gas
MCC of visceral ischemia
- Embolic occlusion: 50%
- Thrombotic occlusion: 25%
- Nonocclusive: 15%
- Venous thrombosis: 5%
MC location of SMA embolism
Most commonly occurs near origin of SMA
#1 source of SMA embolism
Heart (atrial fibrillation)
- Pain out of proportion to exam; pain usually of sudden onset; hematochezia and peritoneal signs are late findings
- May have h/o a fib, endocarditis, recent MI, recent angiography
Dx / Tx: SMA embolism
Dx: angiogram or abdominal CT with IV contrast
Tx: embolectomy, resect infarcted bowel if present
How do you expose the SMA?
Divide ligament of Treitz, SMA is to the right of this near the base of the transverse colon mesentery
- Often history of chronic problems (food fear, weight loss)
- Possible history of vasculitis or hyper coagulable state
- Symptoms: similar to embolism, may have developed some collaterals
Dx / Tx SMA thrombosis
Dx: angiogram or abdominal CT with IV contrast
Tx: thrombectomy (open or catheter directed; thrombolytics may have a role) ; may need PTA with stent or open bypass after the vessel is opened for any residual stenosis; resection of infarcted bowel
Dx: SMA thrombosis
Angiogram or abdominal CT with IV contrast
Tx: SMA thrombosis
thrombectomy (open or catheter directed; thrombolytics may have a role) ; may need PTA with stent or open bypass after the vessel is opened for any residual stenosis; resection of infarcted bowel
- Usually short segments of intestine involved; bloody diarrhea, crampy abdominal pain
- May have a history of vasculitis, hyper coagulable state, portal HTN
Mesenteric vein thrombosis
Dx: mesenteric vein thrombosis
Abdominal CT scan or angiogram with venous phase
Tx: mesenteric vein thrombosis
Heparin usual; resection of infarcted bowel if present
Dx / Tx: mesenteric vein thrombosis
Dx: abdominal CT scan or angiogram with venous phase
Tx: heparin usual; resection of infarcted bowel if present
- Spasm, low-flow states, hypovolemia, hemoconcentration, digoxin -> final common pathway is low cardiac output to visceral vessels
- Symptoms: bloody diarrhea, pain
Nonocclusive mesenteric ischemia
Final common pathway of nonocclusive mesenteric ischemia
Low cardiac output to visceral vessels
Risk factors of nonocclusive mesenteric ischemia
Prolonged shock, CHF, prolonged cardiopulmonary bypass
What areas are most vulnerable to nonocclusive mesenteric ischemia?
Watershed areas (Griffith's - splenic flexure and Sudak's - upper rectum)
Watershed area: splenic flexure
Watershed area: upper rectum
Tx: nonocclusive mesenteric ischemia
Volume resuscitation, catheter-directed nitroglycerin can increase visceral blood flow; also need to increase cardiac output (dobutamine); resection of infarcted bowel if present
- Causes celiac artery compression
- Bruit near epigastrium, chronic pain, weight loss, diarrhea
Median arcuate ligament syndrome
Tx: median arcuate ligament syndrome
Transect median arcuate ligament; may need arterial reconstruction
Weight loss secondary to food fear (visceral angina 30 minutes after meals)
Chronic mesenteric ischemia
Dx: chronic mesenteric ischemia
Get lateral visceral vessel aortography to see origins of celiac and SMA
Tx: chronic mesenteric ischemia
PTA and stent; bypass if that fails
Important collateral between the SMA and celiac
Arc of Riolan
Most common complication of aneurysms above the inguinal ligament
Most common complications of aneurysms below inguinal ligament
Thrombosis and emoli
Risk factors for visceral artery aneurysms
Medial fibrodysplasia, portal HTN, arterial disruption secondary to inflammatory disease (eg, pancreatitis)
Repair guidelines for visceral artery aneursyms
Repair all splanchnic artery aneurysms (>2cm) when diagnosed (50% risk for rupture) except splenic
MC visceral aneurysm
- More common in women
- 2% risk of rupture
Splenic artery aneurysm
When do you repair splenic artery aneurysms?
If symptomatic, if patient is pregnant, if occurs in women of childbearing age, or is > 3-4 cm
Splenic artery aneurysm: what is concerning in pregnants?
High rate of pregnancy-related rupture -> usually in 3rd trimester
Tx: visceral artery aneurysm
Covered stent (best); exclusion with bypass if that fails
Treatment splenic artery aneurysms
Splenic artery aneurysms can just be ligated if open procedure is required (have good collaterals)
When do you treat renal artery aneurysms?
> 1.5 cm
Tx: covered stent
When do you treat iliac and femoral artery aneurysms?
Iliac: > 3.0 cm
Femoral: > 2.5 cm
Tx: covered stent
Most common peripheral aneurysm
Popliteal artery aneurysm
- Leg exam reveals prominent popliteal pulses
- 1/2 are bilateral
- 1/2 have another aneurysm elsewhere (AAA, femoral, etc)
- Most likely to get thrombosis or emboli with limb ischemia
- Can also get leg pain from compression of adjacent structures
Popliteal artery aneurysm
Dx: popliteal artery aneurysm
Surgical indications for repair of popliteal artery aneurysm
Symptomatic, > 2cm, or mycotic
TX: popliteal artery aneurysm
Exclusion and bypass of all popliteal aneurysms; 25% have complication that requires amputation if not treated; covered stent not recommended for these
Collection of blood in continuity with the arterial system but not enclosed by all 3 layers of the arterial wall
Most common location of pseudoaneurysm
What can cause pseudo aneurysm?
Can result from percutaneous interventions or from disruption of a suture line between graft and artery
Treatment pseudo aneurysm if it occurs after percutaneous intervention
Ultrasound-guided compression with thrombin injection (surgical repair if flow remains in the pseudo aneurysm after thrombin injection)
Treatment pseudo aneurysm if it occurs at a suture line early after surgery
Need surgical repair
What do pseudo aneurysms that occur at suture lines late after surgery (months to years) suggest?
Suggests graft infection
- Young women; HTN if renal involved; headaches or stroke if carotids involved
- String of beads appearance
Most commonly involved vessel in fibromuscular dysplasia
Renal artery, followed by carotid and iliac
Most common variant of fibromuscular dysplasia
- young men, smokers
- severe rest pain with bilateral ulceration; gangrene of digits, especially fingers
What do you see on arteriogram of Buerger's disease?
Corkscrew collaterals on angiogram and severe distal disease; normal arterial tree proximal to popliteal and brachial vessels (i.e., a small vessel disease)
Treatment: Buerger's disease
Stop smoking of will require continued amputations
Cystic medial necrosis syndromes
Marfan's, Ehlers-Danlos syndrome
Fibrillin defect (connective tissue elastic fibers); marfanoid habitus, retinal detachment, aortic root dilatation
- Many types of collagen defects are identified
- Easy bruising, hypermobile joints; tendency for arterial rupture, especially abdominal vessels
- Get aneurysms and dissections
Angiogram protocol for Ehlers Danlos syndrome
No angiograms -> risk of laceration to vessel
What is important to consider in Ehlers Danlos syndrome cystic medial necrosis?
Often too difficult to repair and need ligation of vessels to control hemorrhage
- Women, age > 55, headache, fever, blurred vision (risk of blindness)
- Inflammation of large vessels (aorta and branches)
- Long segments of smooth stenosis alternating with segments of larger diameter
Temporal arteritis (large artery)
What do you see on temporal artery biopsy in temporal arteritis?
Giant cell arteritis, granuloma
What do you see on temporal artery biopsy in temporal arteritis?
Giant cell arteritis, granuloma
Tx: temporal arteritis (large artery)
Steroids, bypass of large vessels if needed; no endarterectomy
- Weight loss, rash, arthralgias, HTN, kidney dysfunction
- Get aneurysms that thromboses or rupture
- Renals most commonly involved
Polarteritis nodosa (medium artery)
What organ is most commonly involved in polyarteritis nods?
Tx: polyarteritis nodosa (medium artery)
- Children; febrile viral illness with erythematous mucosa and epidermis
- Get aneurysms of coronary arteries and brachiocephalic vessels
- Die from arrhythmias
Kawasaki's disease (medium artery)
What do peeps with Kawasaki's die from?
Tx: kawasaki disease
Steroids, possible CABG
- Often secondary to drug / tumor antigens
- Symptoms: rash (palpable purpura), fever, symptoms of end-organ dysfunction
Hypersensitivity angiitis (small artery)
Tx: hypersensitivity angiitis (small artery)
Calcium channel blockers, pentoxifylline, stop offending agent
- Late late
- Early: sloughing and thrombosis (obliterative endarteritis)
- Late: (1-10 years) - fibrosis, scar, stenosis
- Late late (3-30 years) - advanced atherosclerosis
- Young women
- Pallor -> cyanosis -> rubor
Tx: raynaud's disease
Calcium channel blockers, warmth
Joins femoral vein near groin; runs medially
Greater saphenous vein
Why no clamps on the IVC?
Can be ligated near the IVC in emergencies because of collaterals (left gonadal vein, left adrenal vein); right renal vein does not have these collaterals
Left renal vein
Most common failure of AV grafts for dialysis
Venous obstruction secondary to intimal hyperplasia
Dialysis access grafts:
- Radial artery to cephalic vein
- Wait 6 weeks to use -> allows vein to mature
Dialysis access grafts
- eg brachiocephalic loop graft
- wait 6 weeks to allow fibrous scar to form
Two types of dialysis access graft
Cimino, interposition graft
- Usually secondary to trauma; can get peripheral arterial insufficiency, CHF, aneurysm, limb-length discrepancy
- Most need repair -> lateral venous suture; arterial side may need patch or bypass graft; try to place interposing tissue so it does not recure
Acquired AV fistula
- Causes: smoking, obesity, low activity
- Tx: sclerotherapy
- Secondary to venous valve incompetence (90%)
- Ulceration occurs above and posterior to malleoli
Venous ulcers: size that often heal without surgery
Ulcers > 3cm often heal without surgery
Tx: venous ulcers
Unna boot compression cures 90%
What do you need to consider in the treatment of venous ulcers?
May need to ligate perforators or have vein stripping of greater saphenous vein
- Aching, swelling, night cramps, brawny edema, venous ulcers
- Elevation brings relief
What causes edema in venous insufficiency?
Secondary to incompetent perforators and/or valves
Tx: venous insufficiency
Leg wraps, ambulation with avoidance of long standing
Treatment of venous ulcers: for severe symptoms or recurrent ulceration despite medical treatment
Greater saphenous vein stripping (for saphenofemoral valve incompetence) or removal or perforators (if just perforator valves are incompetent; stab avulsion technique)
- Tx: NSAIDs, warm packs, ambulation
- Pus fills vein; fever, increased WBCs, erythema, fluctuant; usually associated with infection following a peripheral IV
- Tx: resect entire vein
What is associated with migrating thrombophlebitis?
Augmentation of flow with distal compression or release of proximal compression
Normal venous Doppler ultrasound
Help prevent blood clots by decreasing venous stasis and increasing tPA release
Sequential compression devices (SCDs)
- Most common in calf
- Pain, tenderness, calf swelling
- Risk factors: Virchow's triad (venous stasis, hypercoaguability, venous wall injury)
Why is the left leg 2x more involved than right in DVT?
Longer left iliac vein compressed by right iliac artery
DVT: minimal swelling
DVT: ankle and calf swelling
DVT: leg swelling
Tenderness, pallor (whiteness), edema
- Tx: heparin
Phlegmasia alba dolens
Tenderness, cyanosis (blueness), massive edema
- Tx: heparin, rarely need surgery
Phlegmasia alba dolens
IVC filter indications
Contraindication to anticoagulation; PE while on coumadin; free-floating ileofemoral thrombi; after pulmonary embolectomy
Etiology of pulmonary embolism with filter in place
Comes from ovarian veins, inferior vena cava superior to filter, or from upper extremity via the superior vena cava
Treatment: venous thrombosis with central line
Pull out central line if not needed, then heparin; can try to treat with systemic heparin or TPA down line if the access site is important
- Do not contain a basement membrane
- Not found in bone, muscle, tendon, cartilage, brain, or cornea
Are lymphatics valveless?
Deep lymphatics have valves
- Occurs when lymphatics are obstructed, too few in number, or nonfunctional
- Leads to woody edema secondary to fibrosis in subcutaneous tissue (toes, feet, ankle, leg)
What are big problems in lymphedema?
Cellulitis and lymphangitis secondary to minor trauma are big problems
Most common infection in lymphedema
Laterality of congenital lymphedema
L > R
Leg elevation, compression, antibiotics for infections
Raised blue/red coloring; early metastases to lung
Lymphangiosarcoma associated with breast axillary dissection and chronic lymphedema
- Usually after dissection in the groin (e.g. after femoral to popliteal bypass)
- Leakage of clear fluid
Percutaneous drainage (can try a couple of times); resection if that fails