– Vascular

Most common congenital hypercoagulable disorder – resistance to activated protein C (Leiden factor)

Most common acquired hypercoagulable disorder – smoking

ATHEROSCLEROSIS STAGES

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: smoking, HTN, hypercholesterolemia, DM, hereditary factors

CEREBROVASCULAR DISEASE

Stroke 3rd most common cause of death in the United States

HTN – most important risk factor for stroke

Carotids supply 85% of blood flow to brain

• Carotid bifurcation – most common site of stenosis

Normal internal carotid artery (ICA) has continuous forward flow

• 1st branch of internal carotid artery – ophthalmic artery

Normal external carotid artery (ECA) has triphasic flow

• 1st branch of external carotid artery – superior thyroid artery

Communication between the ICA and ECA occurs through the ophthalmic artery (off ICA) and internal maxillary artery (off ECA)

Middle cerebral artery – most commonly diseased intracranial artery

Cerebral ischemic events – most commonly from arterial embolization from the ICA (not thrombosis)

• Can also occur from a low-flow state through a severely stenotic lesion

• Heart is the 2nd most common source of cerebral emboli

Anterior cerebral artery events – mental status changes, release, slowing

Middle cerebral artery events – contralateral motor and speech (if dominant side); contralateral facial droop

Posterior cerebral artery events – vertigo, tinnitus, drop attacks, incoordination

Amaurosis fugax – occlusion of the ophthalmic branch of the ICA (visual changes → shade coming down over eyes); visual changes are transient

• See Hollenhorst plaques on ophthalmologic exam

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

Carotid endarterectomy (CEA)

• Repair indications: symptomatic > 70% stenosis, asymptomatic > 80% stenosis

• Recent completed stroke → wait 4–6 weeks and then perform CEA if it meets criteria (bleeding risk if performed earlier)

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

• Use a shunt during CEA for stump pressures < 50 or if contralateral side is tight

• Repair the tightest side first if the patient has bilateral stenosis

• Repair the dominant side first if the patient has equally tight carotid stenosis bilaterally

• Complications from repair

• Vagus nerve injury – most common cranial nerve injury with CEA → secondary to vascular clamping during endarterectomy; patients get hoarseness (recurrent laryngeal nerve comes off vagus)

• Hypoglossal nerve injury – tongue deviates to the side of injury → speech and mastication difficulty

• Glossopharyngeal nerve injury – rare; occurs with really high carotid dissection → causes difficulty swallowing

• Ansa cervicalis – innervation to strap muscles; no serious deficits

• Mandibular branch of facial nerve – affects corner of mouth (smile)

• Acute event immediately after CEA → back to OR to check for flap or thrombosis

• Pseudoaneurysm – pulsatile, bleeding mass after CEA; Tx: drape and prep before intubation, intubate, then repair

• 20% have hypertension following CEA – caused by injury to carotid body; Tx: Nipride to avoid bleeding

• Myocardial infarction – most common cause of non-stroke morbidity and mortality following CEA

• 15% restenosis rate after CEA

• Carotid stenting – for high-risk patients (eg patients with previous CEA and restenosis, multiple medical comorbidities, previous neck XRT)

Vertebrobasilar artery disease

• Anatomy: the 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.

• Usually need basilar artery or bilateral vertebral artery disease to have symptoms

• Caused by atherosclerosis, spurs, bands; get vertebrobasilar insufficiency

• Symptoms: diplopia, vertigo, tinnitus, drop attacks, incoordination

• Tx: PTA with stent

Carotid body tumors – present as a painless neck mass, usually near bifurcation, neural crest cells; are extremely vascular; Tx: resection

THORACIC AORTIC DISEASE

Anatomy – aortic arch vessels include the innominate artery (which branches into the right subclavian and right common carotid arteries), the left common carotid artery, and the left subclavian artery

Ascending aortic aneurysms

• Often asymptomatic and picked up on routine CXR

• Can get compression of vertebra (back pain), RLN (voice changes), bronchi (dyspnea or PNA), or esophagus (dysphagia)

• Indications for repair: acutely symptomatic, ≥ 5.5 cm (with Marfan’s > 5.0 cm), or rapid ↑ in size (> 0.5 cm/yr)

Descending aortic aneurysms (also thoracoabdominal aneurysms)

• Indications for repair

• If endovascular repair possible – > 5.5 cm

• If open repair needed – > 6.5 cm

• Risk of mortality or paraplegia is less with endovascular repair (2%–3%) compared to open repair (20%)

• Reimplant intercostal arteries below T8 to help prevent paraplegia with open repair

Aortic dissections

• Stanford classification – based on presence or absence of involvement of ascending aorta

• Class A – any ascending aortic involvement

• Class B – descending aortic involvement only

• DeBakey classification – based on the site of tear and extent of dissection

• Type I – ascending and descending

• Type II – ascending only

• Type III – descending only

• Most dissections start in the ascending aorta

• Can mimic myocardial infarction

• Symptoms: tearing-like chest pain; can have unequal pulses (or BP) in upper extremities

• 95% of patients have severe HTN at presentation

• Other risk factors: Marfan’s syndrome, previous aneurysm, atherosclerosis

• CXR – usually normal; may have wide mediastinum

• Dx: chest CT with contrast

• Dissection occurs in medial layer of blood vessel wall

• Aortic insufficiency occurs in 70%, caused by annular dilatation or when aortic valve cusp is sheared off

• Can also have occlusion of the coronary arteries and major aortic branches

• Death with ascending aortic dissections usually secondary to cardiac failure from aortic insufficiency, cardiac tamponade, or rupture

• Medical Tx initially → control BP with IV β-blockers (eg esmolol) and Nipride

• Tx:

• Operate on all ascending aortic dissections – Tx: need open repair; graft is placed to eliminate flow to the false lumen

• 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 these patients with lifetime serial scans (MRI to decrease radiation exposure); 30% eventually get aneurysm formation requiring surgery

• Postop complications for thoracic aortic surgery – MI, renal failure, paraplegia (descending thoracic aortic surgery)

• Paraplegia caused by spinal cord ischemia due to occlusion of intercostal arteries and artery of Adamkiewicz that occurs with descending thoracic aortic surgery

ABDOMINAL AORTIC DISEASE

Abdominal aortic aneurysms (AAAs)

• Normal aorta 2–3 cm

• Result from degeneration of the medial layer

• Risk factors: males, age, smoking, family history

• Usually found incidentally

• Can present with rupture, distal embolization, or compression of adjacent organs

• Rupture

• Leading cause of death without an operation

• Symptoms: back or abdominal pain; can have profound hypotension

• Dx: ultrasound or abdominal CT

• CT shows fluid in retroperitoneal space and extraluminal contrast with rupture

• Most likely to rupture on left posterolateral wall, 2–4 cm below renals

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

• 50% mortality with rupture if patient reaches hospital alive

• Tx: repair if symptomatic, > 5.5 cm, or growth > 0.5 cm/yr

• Reimplant inferior mesenteric artery (IMA) if backpressure < 40 mm Hg (ie poor backbleeding), previous colonic surgery, stenosis at the superior mesenteric artery, or flow to left colon appears inadequate

• Ligate bleeding lumbar arteries

• Usually use a straight tube Dacron graft for repair of AAAs

• If performing an aorto-bifemoral repair instead of a straight tube graft, you should ensure flow to at least one internal iliac artery (hypogastric artery) to avoid vasculogenic impotence

• Complications:

• Major vein injury with proximal cross-clamp – retro-aortic left renal vein

• Impotence in ⅓ secondary to disruption of autonomic nerves and blood flow to the pelvis

• 5% mortality with elective repair

• #1 cause of acute death after surgery – MI

• #1 cause of late death after surgery – renal failure

• RFs for mortality – creatinine > 1.8 (#1), CHF, EKG ischemia, pulmonary dysfunction, older age, females

• Graft infection rate – 1%

• Pseudoaneurysm after graft placement – 1%

• Atherosclerotic occlusion – most common late complication after aortic graft placement

• Diarrhea (especially bloody) after AAA repair worrisome for ischemic colitis:

• Inferior mesenteric artery (IMA) often sacrificed with AAA repair and can cause ischemia (most commonly the left colon)

• Dx: endoscopy or abdominal CT; middle and distal rectum are spared from ischemia (middle and inferior rectal arteries are branches off internal iliac artery)

• 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

Inflammatory aneurysms

• Occurs in 10% of patients with AAA; males

• Not secondary to infection – just an inflammatory process

• Can get adhesions to the 3rd and 4th portions of the duodenum

• Ureteral entrapment in 25%

• Weight loss, ↑ ESR, thickened rim above calcifications on CT scan

• May need to place preoperative ureteral stents to help avoid injury

• Inflammatory process resolves after aortic graft placement

Mycotic aneurysms

• Salmonella #1, Staphylococcus #2

• Bacteria infect atherosclerotic plaque, cause aneurysm

• Pain, fevers, positive blood cultures in 50%

• Periaortic fluid, gas, retroperitoneal soft tissue edema, lymphadenopathy

• Usually need extra-anatomic bypass (axillary–femoral with femoral-to-femoral crossover) and resection of infrarenal abdominal aorta to clear infection

Aortic graft infections

• Staphylococcus #1, E. coli #2

• See fluid, gas, thickening around graft

• Blood cultures negative in many patients

• Tx: bypass through non-contaminated field (eg axillary-femoral bypass with femoral-to-femoral crossover) and then resect the infected graft

• More common with grafts going to the groin (eg aorto-bifemoral grafts)

Aortoenteric fistula

• Usually occurs > 6 months after abdominal aortic surgery

• Herald bleed with hematemesis, then blood per rectum

• Graft erodes into 3rd or 4th portion of duodenum near proximal suture line

• Tx: bypass through non-contaminated field (eg axillary-femoral bypass with femoral-to-femoral crossover), resect graft, and then close hole in the duodenum

PERIPHERAL ARTERIAL DISEASE (PAD)

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

Signs of PAD – pallor, dependent rubor, hair loss, slow capillary refill

• Most commonly due to atherosclerosis

Statin drugs (lovastatin) – #1 preventive agent for atherosclerosis

Homocystinuria can ↑ risk of atherosclerosis; Tx: folate and B₁₂

Claudication: medical therapy first → ASA, smoking cessation, exercise until pain occurs to improve collaterals

Symptoms occur one level below occlusion:

• Buttock claudication – aortoiliac disease

• Mid-thigh claudication – external iliac

• Calf claudication – common femoral artery or proximal superficial femoral artery disease

• Foot claudication – distal superficial femoral artery or popliteal disease

Lumbar stenosis can mimic claudication

Diabetic neuropathy can mimic rest pain

Leriche syndrome

• No femoral pulses

• Buttock or thigh claudication

• Impotence (from ↓ flow in the internal iliacs)

• Lesion at aortic bifurcation or above

• Tx: aorto-bifemoral bypass graft

Most common atherosclerotic occlusion in lower extremities – Hunter’s canal (distal superficial femoral artery exits here); the sartorius muscle covers Hunter’s canal

Collateral circulation – forms from abnormal pressure gradients

• Circumflex iliacs to subcostals

• Circumflex femoral arteries to gluteal arteries

• Geniculate arteries around the knee

Postnatal angiogenesis – budding from preexisting vessels; angiogenin involved

Ankle–brachial index (ABI)

• < 0.9 – start to get claudication (typically occurs at same distance each time)

• < 0.5 – start to get rest pain (usually across the distal arch and foot)

• < 0.4 – ulcers (usually starts in toes)

• < 0.3 – gangrene

• ABIs can be very inaccurate 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 (ie resting ABI may be 0.9 but can drop to < 0.6 with exercise, resulting in pain)

Pulse volume recordings (PVRs) – used to find significant occlusion and at what level

Arteriogram is indicated if PVRs suggest significant disease – can also at times treat the patient with percutaneous intervention; gold standard for vascular imaging

Surgical indications for PAD – rest pain, ulceration or gangrene, lifestyle limitation, atheromatous embolization

• PTFE (Gortex) – only for bypasses above the knee; need to use vein for below the knee bypasses

• Dacron – good for aorta and large vessels

• Aortoiliac occlusive disease – most get aorto-bifemoral repair

• 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 to prevent vasculogenic impotence and pelvic ischemia

• Isolated iliac lesions – PTA with stent 1st choice; if that fails, consider femoral-to-femoral crossover

• Femoropopliteal grafts

• 75% 5-year patency

• Improved patency rate with surgery for claudication as opposed to limb salvage

• Popliteal artery exposure below knee – posterior muscle is gastrocnemius and anterior muscle is popliteus

• Femoral-distal grafts (peroneal, anterior tibial, or posterior tibial artery)

• 50% 5-year patency; patency not influenced by level of distal anastomosis

• Distal lesions more limb threatening because of lack of collaterals

• Bypasses to distal vessels are usually used only for limb salvage

• Bypassed vessel needs to have run-off below the ankle for this to be successful

• Synthetic grafts have decreased patency below the knee → need to use saphenous vein

• Extra-anatomic grafts can be used to avoid hostile conditions in the abdomen (multiple previous operations in a frail patient)

• Femoral-to-femoral crossover graft – doubles blood flow to donor artery; can get vascular steal in donor leg

Swelling following lower extremity bypass:

• Early – reperfusion injury and compartment syndrome (Tx: fasciotomies)

• Late – DVT (Dx: U/S, Tx: heparin, Coumadin)

Complications of reperfusion of ischemic tissue – compartment syndrome, lactic acidosis, hyperkalemia, myoglobinuria

Technical problem – #1 cause of early failure of reversed saphenous vein grafts

Atherosclerosis – #1 cause of late failure of reversed saphenous vein grafts

Patients with heel ulceration to bone → Tx: amputation

Dry gangrene – noninfectious; can allow to autoamputate if small or just toes

• Large lesions should be amputated

• See if patient has correctable vascular lesion

Wet gangrene – infectious; need to remove infected necrotic material; antibiotics

• Can be a surgical emergency if extensive infection (eg swollen red toe with pus coming out and red streaks up leg) or systemic complications occur (eg septic) – may need emergency amputation

Mal perforans ulcer

• At metatarsal heads – 2nd MTP joint most common

• Diabetics; can have osteomyelitis

• Tx: non-weightbearing, debridement of metatarsal head (need to remove cartilage), antibiotics; assess need for revascularization

Percutaneous transluminal angioplasty (PTA)

• Excellent for common iliac artery stenosis

• Best for short stenoses

• Intima usually ruptured and media stretched, pushes the plaque out

• Requires passage of wire first

Compartment syndrome

• Is caused by reperfusion injury to the extremity (mediated by PMNs; occurs with cessation of blood flow to extremity and reperfusion > 4–6 hours later)

• Reperfusion injury leads to swelling of the muscle compartments → raising compartment pressures, which can lead to ischemia

• Symptoms: pain with passive motion; extremity feels tight and swollen

• Most likely to occur in the anterior compartment of leg (get foot drop)

• Dx: often based on clinical suspicion; compartment pressure > 20–30 mm Hg abnormal

• Tx: fasciotomies (get all 4 compartments if in lower leg) → leave open 5–10 days

Popliteal entrapment syndrome