Major presentations

Peripheral arterial disease and claudication

PAD is atherosclerotic narrowing of the limb arteries. It runs on a spectrum from asymptomatic, through intermittent claudication, to chronic limb-threatening ischemia at the severe end.

Intermittent claudication is reproducible exertional muscle pain, cramping or fatigue that is relieved by a few minutes of standing still. It is a quality-of-life problem with a low rate of limb loss (on the order of 1 to 2 percent a year). The real danger to these patients is their coexisting coronary and cerebrovascular disease, which is why every claudicant is a cardiovascular risk-reduction patient first.

The two historical staging systems are worth knowing because attendings switch between them freely.

Management is medical first

• Risk-factor therapy for everyone. Smoking cessation, a high-intensity statin, an antiplatelet, and control of blood pressure and diabetes. Low-dose rivaroxaban (2.5 mg twice daily) with aspirin is an option in selected patients to cut limb and cardiovascular events. Details are in Foundations.
• Supervised exercise therapy. First-line for walking distance, and it rivals revascularization for claudication. Cilostazol adds a modest benefit if there is no heart failure.
• Revascularization only for lifestyle-limiting symptoms that persist despite medical therapy and exercise, in a patient who understands the trade-off. The choice between endovascular and open repair depends on the location and length of the disease. Interventions below the knee for claudication alone are generally discouraged, because durability is poor and failure can make the limb worse.

Chronic limb-threatening ischemia

CLTI, the modern term for "critical limb ischemia," is the severe end of PAD: ischemic rest pain for more than two weeks, a non-healing ulcer, or gangrene, together with objectively reduced perfusion.

Rest pain is classically in the forefoot and toes, worse lying flat at night, and relieved by hanging the foot off the bed, because gravity restores a trickle of perfusion. Many patients sleep in a chair. Ask about it specifically, because they rarely volunteer it.

GLASS (the Global Limb Anatomic Staging System) is the anatomic partner to WIfI. It grades the femoropopliteal and infrapopliteal disease along a chosen target artery path, to estimate how likely an endovascular approach is to succeed. Together, WIfI and GLASS frame the patient, the limb and the anatomy, the structure used by the Global Vascular Guidelines.

What the trials changed

• BEST-CLI (2022). In patients with an adequate single-segment great saphenous vein, a surgical bypass-first strategy led to fewer major adverse limb events or deaths than an endovascular-first strategy. Without good vein, the two strategies performed similarly. This revived vein bypass in the right patient and made vein mapping a routine part of the workup.
• BASIL-2 (2023). For CLTI needing an infrapopliteal revascularization, a best-endovascular-first strategy gave better amputation-free survival than vein bypass first, driven mainly by fewer deaths. It applies to a different, more distal population than BEST-CLI.

The practical upshot is individual: the patient's risk, the limb's WIfI stage, the anatomy, and the availability of good vein all shape the choice. CLTI demands revascularization wherever feasible, plus aggressive wound care, offloading and infection control.

Acute limb ischemia Emergency

ALI is a sudden loss of arterial perfusion that threatens limb viability, presenting within two weeks of onset. Muscle tolerates roughly 4 to 6 hours of severe ischemia before irreversible injury begins.

Embolic or thrombotic: the central distinction

The mechanism changes the operation, so this comparison is asked relentlessly.

Rutherford classification of ALI

This is the table that decides what happens next.

Management

1. Anticoagulate immediately. A systemic heparin bolus and infusion the moment ALI is suspected, unless contraindicated, to stop clot propagation. Do not wait for imaging.
2. Grade the limb. The Rutherford class decides the path: I and IIa allow time for CTA and possibly catheter-directed therapy; IIb needs revascularization now, usually in the OR; III is not salvageable.
3. Revascularize. Balloon embolectomy with a Fogarty catheter (classic for embolic disease), catheter-directed thrombolysis or mechanical thrombectomy (often suited to thrombotic disease and category I to IIa limbs), surgical bypass, or a hybrid of these.
4. Anticipate reperfusion. Restoring flow to ischemic muscle releases potassium, myoglobin and acid. Watch for hyperkalemia, rhabdomyolysis, acute kidney injury and compartment syndrome, and keep a low threshold for fasciotomy.
5. Find the source. After an embolus: ECG and telemetry for atrial fibrillation, an echocardiogram, and a plan for long-term anticoagulation.

Abdominal aortic aneurysm

An aneurysm is a focal dilation more than 1.5 times the normal vessel diameter. For the infrarenal aorta that means 3.0 cm or more. Most are infrarenal and degenerative.

Risk factors are smoking (the strongest modifiable one), male sex, older age, a family history in a first-degree relative, and other atherosclerotic disease. Diabetes is, curiously, protective.

Screening and surveillance

The USPSTF recommends a one-time screening ultrasound for men aged 65 to 75 who have ever smoked, with selective screening for men who never smoked. The SVS recommends a broader net: men and women aged 65 to 75 with a smoking history, and people with a first-degree relative with an AAA. Small aneurysms are followed by ultrasound at intervals that shorten as they grow.

When to repair electively

• Diameter of 5.5 cm or more in men.
• Diameter of 5.0 cm or more in women (European guidance; the SVS suggests considering repair from 5.0 to 5.4 cm in women).
• Rapid growth: more than 1 cm in a year, or more than 0.5 cm in six months.
• Symptoms at any size: tenderness, back or abdominal pain attributable to the aneurysm, or distal embolization.

Repair is by EVAR when the anatomy suits it, or open repair. EVAR has lower early mortality, the long-term survival of the two converges, and EVAR needs lifelong imaging surveillance because of endoleak and late failure. Both are covered in Open operations and Endovascular.

Variants to recognize

Inflammatory AAA

A thick, inflamed wall with a peri-aortic rind, raised inflammatory markers, often pain, and classically ureteral entrapment. The inflammation often settles after repair.

Mycotic (infected) AAA

Saccular, often in an unusual location, rapidly expanding, in a febrile patient. Salmonella and Staphylococcus are classic organisms. Needs prolonged antibiotics and repair, with attention to infected-field reconstruction.

Carotid disease and stroke prevention

Plaque at the carotid bifurcation causes stroke mainly by embolization of plaque or thrombus to the brain, and less often by flow limitation from a tight stenosis. The whole point of carotid intervention is stroke prevention, not symptom relief.

Symptomatic or asymptomatic

Symptomatic disease means an ipsilateral neurologic event in the previous six months: a TIA, a stroke, or amaurosis fugax (transient monocular blindness, "a curtain coming down," from a retinal artery embolus). Asymptomatic disease is found on screening or because of a bruit.

Indications, and what the trials showed

NASCET and ECST established the benefit of endarterectomy for symptomatic stenosis. ACAS and ACST-1 showed a smaller benefit in asymptomatic patients, in an era before modern medical therapy.

CREST-2 (reported in 2025) compared intensive medical management alone with revascularization plus intensive medical management in asymptomatic patients with severe stenosis. In the stenting comparison, adding stenting lowered the rate of stroke; in the endarterectomy comparison, the benefit did not reach statistical significance. How this changes practice for asymptomatic disease is still being worked out, so expect your attendings to discuss it and guidelines to move.

Endarterectomy, transfemoral stenting or TCAR

Carotid endarterectomy remains the reference standard. Transfemoral carotid stenting is an alternative, particularly for a hostile neck (prior radiation or neck surgery, a high lesion) or high surgical risk, but CREST showed stenting carried more periprocedural strokes and surgery more myocardial infarctions, with stenting faring worse in older patients. Transcarotid artery revascularization (TCAR) uses a small incision at the base of the neck, direct carotid access and flow reversal for embolic protection, avoiding the aortic arch, and has become a widely used middle path. The operations are described in Open operations.

Mesenteric ischemia

Reduced blood flow to the gut, split into an acute emergency and a chronic, indolent form. The vessels at stake are the celiac trunk, the SMA and the IMA.

Acute mesenteric ischemia Emergency

The hallmark is pain out of proportion to the exam: a patient in severe abdominal pain with a soft, relatively benign-feeling abdomen early on. Peritonitis, bloody stool and shock are late signs that usually mean dead bowel.

The workup shows leukocytosis, a rising lactate and a metabolic acidosis, although a normal lactate early does not exclude it. CTA is the imaging test of choice. Management is to resuscitate, start heparin, give broad-spectrum antibiotics, revascularize urgently (embolectomy, bypass, or endovascular stenting, sometimes retrograde through an open SMA), and resect frankly necrotic bowel, with a planned second-look operation at 24 to 48 hours for marginal segments.

Chronic mesenteric ischemia

"Intestinal angina." The triad is postprandial abdominal pain, food fear (sitophobia) and weight loss, in an older patient with vascular disease. Because the collateral network is rich, symptoms usually need significant disease in at least two of the three vessels. Treatment is revascularization, now mostly endovascular stenting of the SMA, with open bypass for selected patients.

Aortic dissection Emergency

A tear in the intima lets blood track into the media, creating a false lumen that can propagate, occlude branch vessels (malperfusion), or rupture.

The presentation is sudden, severe, tearing chest or back pain, sometimes with a pulse or blood pressure difference between the arms, or signs of organ malperfusion: a cold leg, abdominal pain with a rising lactate, falling urine output, or a neurologic deficit.

The 2020 SVS/STS reporting system classifies by the location of the entry tear: type A if it is in zone 0 (the ascending aorta), type B if it is beyond zone 0, with subscripts for the proximal and distal extent by aortic zone (for example B_3,10). A type B tear whose dissection extends back into the arch is written B₀ or B₁ or B₂, the group older papers called "non-A non-B." Chronicity is hyperacute (under 24 hours), acute (1 to 14 days), subacute (15 to 90 days) and chronic (over 90 days). Zones are explained in Endovascular.

Initial medical management

The goal is to reduce the force of each heartbeat on the aortic wall (the rate of rise of pressure) and the pressure itself. Start an IV beta-blocker first (esmolol or labetalol), then add a vasodilator such as nicardipine, clevidipine or nitroprusside if the pressure is still high. The 2022 ACC/AHA targets are a heart rate of 60 to 80 and a systolic under 120 mmHg, or the lowest pressure that keeps the brain, kidneys and gut perfused. Older teaching used a heart rate under 60, so confirm the target your attending wants. Treat the pain, place an arterial line, and admit to the CTV ICU.

Type A dissections go to cardiac surgery emergently. Type B dissections are managed medically unless complicated by malperfusion, rupture, rapid expansion, or pain or hypertension that will not settle, in which case TEVAR to cover the entry tear is the usual intervention. Uncomplicated type B dissections with high-risk features (such as a total aortic diameter of 40 mm or more, or a large entry tear) are increasingly considered for TEVAR in the subacute window.

Deep vein thrombosis and venous thromboembolism

Venous thromboembolism spans DVT and pulmonary embolism. Its pathophysiology is captured by Virchow's triad.

Diagnosis combines pretest probability (the Wells score), D-dimer (useful to rule out disease when probability is low) and compression duplex ultrasound, the confirmatory test, which shows a non-compressible vein.

Treatment

• Anticoagulation is the treatment. A direct oral anticoagulant is first-line for most patients, including many with cancer. Low-molecular-weight heparin or warfarin suits others (pregnancy, severe renal failure, antiphospholipid syndrome).
• Duration. About three months for a DVT provoked by a transient risk factor such as surgery. For an unprovoked DVT or a persistent risk factor, extended anticoagulation is considered, balanced against bleeding risk.
• Isolated calf DVT. Either anticoagulate or repeat the ultrasound in one to two weeks to look for extension, depending on symptoms and risk.
• Thrombus removal. Catheter-directed lysis or mechanical thrombectomy for selected patients with acute iliofemoral DVT, severe symptoms and low bleeding risk. ATTRACT (2017) did not reduce post-thrombotic syndrome overall but did reduce its severity, with the best signal in iliofemoral disease; CAVA (2020) found no reduction. So it is a selective, not a routine, therapy.
• IVC filters. The clear indication is acute proximal DVT or PE in a patient who cannot be anticoagulated. Placing a filter for recurrent PE despite anticoagulation is debated, and PREPIC2 found no benefit from adding a filter to anticoagulation. Plan the retrieval when the filter goes in.

Chronic venous insufficiency and varicose veins

When venous valves fail, blood refluxes and venous pressure stays high (venous hypertension), producing varicose veins, heaviness, edema, skin changes and ultimately ulceration.

Venous or arterial ulcer?

Management

Treatment starts with compression and elevation. For refluxing superficial veins, the options are endovenous thermal ablation (radiofrequency or laser), non-thermal ablation (cyanoacrylate glue or mechanochemical ablation), foam sclerotherapy, and phlebectomy for the varicosities themselves. For a venous ulcer, the EVRA trial (2018) showed that early ablation of superficial reflux, added to compression, healed ulcers faster and reduced recurrence. After thermal ablation, a duplex looks for endovenous heat-induced thrombosis (EHIT) extending toward the deep vein.

The diabetic foot

Diabetic foot disease is the convergence of three processes: neuropathy, ischemia and infection. Each worsens the others, and together they make the diabetic foot the leading cause of non-traumatic amputation.

• Neuropathy. Loss of protective sensation leads to unnoticed trauma. Neuropathic ulcers sit under pressure points (metatarsal heads, heel) in a foot that may have intact circulation.
• Ischemia. Diabetic PAD favors the tibial vessels below the knee, often sparing the foot arteries, and calcification can make the ABI falsely high, so use toe pressures.
• Infection. Can spread fast along tendon sheaths and compartments with surprisingly little systemic response. A deep space infection or wet gangrene is a surgical emergency for drainage first.
• Charcot foot. Progressive neuropathic joint destruction producing the collapsed "rocker-bottom" foot. In the acute phase it can mimic infection (red, hot, swollen) without a wound.

Severity is staged with WIfI, which has largely replaced older systems such as Wagner and the University of Texas classification for limb-threat decisions. A positive probe-to-bone test suggests osteomyelitis; X-ray and then MRI help confirm it.

Other key presentations

Briefer, but each is a known consult and a known question.

Popliteal artery aneurysm clots, not ruptures

The most common peripheral aneurysm. The danger is thrombosis and distal embolization causing limb loss, not rupture. Often bilateral and associated with an AAA, so image the other knee and the aorta. Repair is generally offered at about 2 cm or more, or with mural thrombus or symptoms at any size.

Splenic and other visceral aneurysms pregnancy risk

The splenic artery is the most common visceral aneurysm, with a female predominance and a notable risk of rupture in pregnancy. Treat at about 3 cm or more, and at smaller sizes in women who are or may become pregnant. Visceral pseudoaneurysms (after pancreatitis or trauma) are treated at any size, usually by embolization.

Renal artery stenosis two populations

Atherosclerotic (older patients, ostial lesions) and fibromuscular dysplasia (younger women, a "string of beads" in the mid vessel). Can cause renovascular hypertension and flash pulmonary edema. CORAL found no routine benefit from stenting atherosclerotic disease, so intervention is selective; FMD is treated with balloon angioplasty without a stent.

Fibromuscular dysplasia

A non-atherosclerotic arteriopathy of medium arteries, mainly renal and carotid or vertebral. It can cause dissections and aneurysms elsewhere, so patients are imaged from head to pelvis once.

Thoracic outlet syndrome three types

Neurogenic (most common, brachial plexus compression). Venous: Paget-Schroetter "effort thrombosis" of the subclavian vein, treated with thrombolysis then first rib resection. Arterial (rarest): subclavian aneurysm or stenosis from a cervical rib, with embolization to the hand. Decompression usually means first rib resection.

Subclavian steal the arm steals from the brain

A proximal subclavian stenosis causes reversed flow down the vertebral artery to feed the arm, giving posterior circulation symptoms with arm exercise and an arm-to-arm blood pressure difference. More common on the left.

Atheroembolism blue toe

Cholesterol crystals showered from an aortic or iliac plaque, often after a catheterization: painful blue toes with palpable pulses, livedo reticularis, sometimes kidney injury and eosinophilia. Find and treat the source, statin and antiplatelet; anticoagulation does not help.

Buerger disease young smoker, digits

Thromboangiitis obliterans: inflammatory, non-atherosclerotic occlusion of small and medium vessels in young smokers, causing digital ischemia and ulcers. The only treatment that works is complete abstinence from tobacco, including nicotine replacement in some patients.

Popliteal entrapment young athlete

An abnormal relationship between the popliteal artery and the gastrocnemius (or popliteus) compresses flow with exercise. Suspect it in a fit young person with calf claudication and normal pulses at rest that fade with plantar flexion.

Vascular trauma hard and soft signs

Hard signs (pulsatile bleeding, an expanding hematoma, a bruit or thrill, an absent pulse, distal ischemia) go to the OR. Soft signs (a diminished pulse, a stable hematoma, proximity to a vessel, a neurologic deficit) get CTA or an injured extremity index (ABI below 0.9 is abnormal).

Large-vessel vasculitis

Takayasu arteritis ("pulseless disease," younger women, aortic arch branches) and giant cell arteritis (over 50, temporal artery, jaw claudication, threat to vision, but also the subclavian and axillary arteries). Avoid operating during active inflammation.

The most common consults, with their first moves, are on Rounds and presenting.