Chapter 27: Vascular Flashcards
Most common congenital hyper coagulable disorder
Resistance to activated protein C (Leiden factor)
Most common acquired hyper coagulable disorder
Smoking
Atherosclerotic stages
- 1st
- 2nd
- 3rd
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
Stroke
Most important risk factor for stroke
HTN
Supple 85% of blood supply to the brain
Carotids
Most common site of stenosis in cerebrovascular disease
Carotid bifurcation
Type of flow from normal internal carotid artery
Continuous forward flow
1st branch off the internal carotid artery
Ophthalmic artery
Type of flow from external carotid artery
Triphasic flow
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
Heart
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
Amaurosis fugax
What do you see on ophthalmologic exam in amaurosis fugax?
Hollenhorst plaques
Treatment: carotid traumatic injury with major fixed deficit:
- Occlusion
- Nonocclusion
- 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
Ansa cervicalis
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
- Treatment?
Pseudoaneurysm
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
Myocardial infarction
Restonosis rate after CEA
15%
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
Tx: resection
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
Stanford classification
DeBakey classification
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
Ascending only
Type III DeBakey
Descending only
Where do most dissections start?
In the ascending aorta
What can aortic dissection mimic?
Myocardial infarction
Symptoms: tearing like chest pain, can have unequal pulses (or BP) in upper extremities
Aortic dissection
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
2-3cm
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
Rupture
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
MI
1 cause of late death after surgery
Renal failure
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
1%
Pseudoaneurysm formation s/p graft placement for AAA repair
1%
Most common later complication after aortic graft placement
Atherosclerotic occlusion
What is diarrhea (especially bloody) worrisome for after AAA repair?
Ischemic colitis
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
- Other
- 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
Inflammatory aneurysms
- 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
#1 Salmonella #2 Staphylococcus
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
Mycotic aneurysms
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
#1 Staphylococcus #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
Aortoenteric fistula
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
Sural nerve
Signs of PAD
Pallor, dependent rubor, hair loss, slow capillary refill
MCC PAD
Atherosclerosis
1 preventative agent for atherosclerosis
Statin drugs (lovastatin)
Can increase risk of atherosclerosis.
- Tx: folate and B12
Homocystinuria
Treatment of claudication
Medical therapy first: ASA, smoking cessation, exercise until pain occurs to improve collaterals
Level of occlusion: buttock claudication
Aortoiliac disease
Level of occlusion: mid-thigh claudication
External iliac
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?
Lumbar stenosis
What can mimic rest pain in PAD?
Diabetic neuropathy
- No femoral pulses
- Buttock or thigh claudication
- Impotence (from decreased flow in the internal iliacs)
Leriche syndrome
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?
Sartorius muscle
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