Questions you'll be asked

The celiac trunk at about T12, the superior mesenteric artery at L1, the paired renal arteries at L1 to L2, and the inferior mesenteric artery at L3, then the bifurcation into the common iliac arteries at about L4. The smaller branches that complete the list are the inferior phrenic, middle adrenal, gonadal and lumbar arteries and the median sacral artery.

Aorta, common iliac, external iliac, then common femoral as it passes under the inguinal ligament, superficial femoral through the adductor canal, popliteal, then the anterior tibial, which becomes the dorsalis pedis on the dorsum of the foot.

Anterior tibial, posterior tibial and peroneal. The dorsalis pedis (the continuation of the anterior tibial) and the posterior tibial, through its plantar branches, form the pedal arch. The peroneal ends above the ankle, but its perforating and communicating branches can reconstitute either vessel. It is often the last tibial vessel spared in a diabetic leg and remains a usable bypass target.

From right to left: the brachiocephalic (innominate) trunk, the left common carotid and the left subclavian. The brachiocephalic divides into the right common carotid and right subclavian. The most common variant is a shared origin of the brachiocephalic and left common carotid, loosely called a bovine arch, which matters when you catheterize the arch or plan a TEVAR landing zone.

The saphenous nerve, along with the nerve to vastus medialis. The superficial femoral artery becomes the popliteal as it leaves the distal end of the canal through the adductor hiatus. Below the knee the saphenous nerve runs with the great saphenous vein, which is why vein harvest or ablation in the calf can leave numbness along the medial leg.

The profunda femoris (deep femoral artery). Its perforating branches, and the descending branch of the lateral circumflex femoral artery, link with the genicular arteries around the knee to reconstitute the popliteal. A healthy profunda can keep a limb viable despite an occluded SFA, which is why it is protected and, when diseased, repaired with a profundaplasty.

• Hypoglossal. The tongue deviates toward the side of the injury, with dysarthria and trouble chewing and swallowing.
• Vagus or recurrent laryngeal. Ipsilateral vocal cord paralysis, with hoarseness and a weak cough. The vagus usually lies posteriorly between the carotid and the jugular and can be caught in a clamp.
• Marginal mandibular branch of the facial nerve. A drooping corner of the mouth, usually from retraction near the angle of the jaw.
• Superior laryngeal. Voice fatigue and loss of high pitch.
• Glossopharyngeal. Dysphagia and aspiration, mainly with a high exposure.
• Greater auricular. Numbness of the earlobe, from a high incision.

Bilateral recurrent laryngeal or hypoglossal injury can obstruct the airway, so cord and tongue function are checked before a staged operation on the other side. See Open operations.

Anterior: the extensors, the deep peroneal nerve and the anterior tibial vessels. Lateral: the peroneus muscles and the superficial peroneal nerve. Superficial posterior: gastrocnemius, soleus and plantaris. Deep posterior: the deep flexors, the posterior tibial and peroneal vessels and the tibial nerve. The anterior compartment is the one most often affected after revascularization, and numbness in the first web space (the deep peroneal nerve) is an early sign. A two-incision fasciotomy releases all four; see Open operations.

At the saphenofemoral junction, where it passes through the saphenous opening (fossa ovalis) into the common femoral vein, a few centimeters below and lateral to the pubic tubercle. It matters because the great saphenous vein is the preferred conduit for both peripheral and coronary bypass, so it is mapped and protected. Before anyone ablates or strips it, someone should ask whether the patient may need it for a bypass later. The junction is also the landmark that decides how a superficial thrombophlebitis is treated (see the venous questions).

A collateral (the meandering mesenteric artery) between the middle colic branch of the SMA and the left colic branch of the IMA, running close to the root of the mesentery. With the marginal artery of Drummond it connects the SMA and IMA territories. A large meandering artery on imaging means one territory is feeding the other because of occlusive disease. If the SMA is occluded and the bowel depends on a patent IMA, ligating or covering that IMA during aortic repair can infarct the bowel, so the IMA may need to be reimplanted.

The common facial vein, which crosses the bifurcation on its way into the internal jugular. It is ligated and divided to expose the bifurcation. The hypoglossal nerve usually crosses the internal and external carotid a short distance above, so dissection heading up the neck from there needs care.

Flow is proportional to the fourth power of the radius and inversely proportional to length and viscosity. A small reduction in lumen diameter causes a large drop in flow, and a slightly larger conduit improves flow a great deal. Halving the radius cuts flow to about one-sixteenth, while doubling the length only halves it, which is why radius dominates.

At roughly a 50 percent reduction in diameter, which is about a 75 percent reduction in cross-sectional area. That is where a measurable pressure and flow gradient appears at rest. With exercise, when distal resistance falls and flow rises, lesser stenoses can become significant, which is why a claudicant can have a normal resting ABI.

Wall tension is proportional to pressure times radius. As an aneurysm enlarges, wall stress climbs at the same blood pressure, which raises rupture risk and drives further expansion, a vicious cycle. It is why diameter is the main predictor of rupture and why blood pressure control matters in anyone with an aneurysm.

For each leg, divide the higher of the dorsalis pedis and posterior tibial systolic pressures by the higher of the two brachial systolic pressures. 1.00 to 1.40 is normal, 0.91 to 0.99 borderline, 0.90 or less diagnostic of PAD, and 0.40 or less severe disease, the range where rest pain and tissue loss are common. Above 1.40 means non-compressible, calcified vessels, so use a toe pressure. CLTI is a clinical diagnosis (rest pain or tissue loss with proven PAD), not an ABI cutoff. The table is in Quick reference.

Medial calcific sclerosis stiffens the tibial arteries so the cuff cannot compress them, and the pressure reads artificially high. The same happens in end-stage kidney disease. The digital arteries are usually spared, so the toe pressure and toe-brachial index are more reliable: a TBI below about 0.70 is abnormal, and a toe pressure under 30 mmHg predicts poor wound healing.

A normal peripheral artery at rest is triphasic: forward flow in systole, brief reversal in early diastole because of high distal resistance, then a small forward component. Loss of the reversal (biphasic) can be normal in older patients or with vasodilation, or can reflect mild disease. A monophasic, dampened signal means significant disease upstream of the probe, even when the signal is loud. Describe the signal at each site rather than writing "dopplerable".

With an exercise (treadmill) ABI. During exercise, a stenosis that was trivial at rest becomes flow-limiting and the ankle pressure falls. A fall in ABI of more than about 20 percent, or in ankle pressure of more than about 30 mmHg, supports PAD; exact criteria vary by lab. If the test is normal, think about the mimics: neurogenic claudication from spinal stenosis, venous claudication, and hip or knee arthritis.

Clamping raises afterload, so proximal pressure and cardiac work rise, which stresses a diseased heart. Unclamping drops afterload suddenly and washes potassium, acid and other metabolites out of the ischemic lower body, causing declamping hypotension. That is why the clamp is released slowly, one limb at a time, with volume on board and anesthesia warned in advance.

About 4 to 6 hours of warm ischemia before irreversible injury. Nerve is more sensitive, which is why sensory loss comes early and motor loss signals a limb in serious trouble; skin tolerates the longest. This is the clock that makes acute limb ischemia an emergency and lowers the threshold for fasciotomy after revascularization.

To reduce the shear force on the wall (the rate of rise of pressure). A vasodilator alone causes reflex tachycardia, which increases shear and can propagate the dissection, so heart rate and contractility are controlled first, usually with IV esmolol or labetalol. The 2022 ACC/AHA targets are a heart rate of 60 to 80 and a systolic pressure under 120 mmHg (older teaching said a heart rate under 60), adding a vasodilator such as nicardipine if needed. See Presentations.

Embolic occlusion is sudden, in a leg with no prior symptoms and normal pulses on the other side, often from atrial fibrillation, and classically lodges at the common femoral bifurcation. Thrombotic occlusion is more gradual, in a patient with known PAD and diseased pulses on both sides, and developed collaterals soften the picture. It matters because an embolus usually goes straight for a Fogarty embolectomy, while a thrombosis on diseased vessels usually needs imaging to plan lysis, endovascular therapy or bypass. The table is in Quick reference.

Give a heparin bolus at once unless contraindicated, call the senior, and revascularize immediately, because a IIb limb is salvageable only with prompt restoration of flow. There is no time for a conventional catheter-directed lytic infusion running over many hours. The options are open embolectomy or thrombectomy, bypass, or rapid endovascular mechanical thrombectomy where the team and suite are ready, and the team should be prepared to do a four-compartment fasciotomy. Category III is irreversible and usually means primary amputation. See On call.

At 5.5 cm in men and 5.0 cm in women (the SVS suggests considering repair in women from 5.0 to 5.4 cm), with rapid growth (1 cm or more in a year; some also use 0.5 cm in six months), or if it becomes symptomatic at any size. Below threshold, the work is surveillance, smoking cessation and cardiovascular risk reduction. Surveillance intervals are in Quick reference.

If unstable, straight to the operating room or hybrid suite with no CT. Use permissive hypotension, keeping the systolic only high enough to keep the patient mentating (often around 70 to 90 mmHg), because aggressive fluid resuscitation can disrupt the contained rupture and worsens coagulopathy. Activate massive transfusion. If the patient is stable enough for a CTA, use it to decide EVAR suitability; endovascular repair is preferred when the anatomy allows, and an aortic occlusion balloon can buy time. The SVS suggests a door-to-intervention time under 90 minutes.

Symptomatic patients (stroke, TIA or amaurosis in the matching territory) with 70 to 99 percent stenosis benefit clearly, and benefit is greatest when they are treated within about two weeks of the event. Symptomatic 50 to 69 percent is a moderate, individualized benefit, and below 50 percent is managed medically. Asymptomatic high-grade disease is treated more selectively: everyone gets intensive medical therapy, and intervention is reserved for selected patients with a good life expectancy and a low procedural risk. CREST-2 (2025) has sharpened this debate; see Landmark trials.

The patient's own great saphenous vein, ideally a single segment, especially for below-knee and tibial targets. When it is absent or inadequate, the alternatives are the other leg's saphenous vein, arm vein or spliced vein. Prosthetic grafts are acceptable for an above-knee femoropopliteal bypass but do poorly below the knee. In BEST-CLI, bypass with an adequate single-segment saphenous vein beat endovascular therapy for CLTI, which is why vein mapping is part of the workup. See Conduits and access.

Chronic limb-threatening ischemia is ischemic rest pain, or tissue loss (a non-healing ulcer or gangrene), present for more than two weeks in a patient with objectively confirmed PAD. The Global Vascular Guidelines stage the limb with WIfI (wound, ischemia and foot infection, each graded 0 to 3), which estimates amputation risk and the likely benefit of revascularization, and describe the arterial anatomy with GLASS to help choose between bypass and endovascular therapy. See WIfI at a glance.

Complicated ones: rupture or impending rupture, or malperfusion of the gut, kidneys, spinal cord or a limb. Most definitions add pain or hypertension that persists despite maximal medical therapy, and rapid expansion. These get TEVAR to cover the entry tear. Uncomplicated type B dissection is treated with anti-impulse therapy and close imaging, and TEVAR is considered when high-risk features are present, such as a large aortic or false-lumen diameter. Type A is a cardiac surgical emergency.

Acute mesenteric ischemia, most often an SMA embolus. Pain out of proportion to the exam is the classic early picture; peritonitis, acidosis and a high lactate come late, and a normal lactate early on should not reassure you. Get a CTA immediately, start heparin, resuscitate, give broad-spectrum antibiotics, and arrange emergent revascularization (open embolectomy or endovascular) with laparotomy to assess the bowel and resect what is dead. A planned second look is common. See Presentations.

Suspect it after any prolonged ischemic time, especially a IIb limb, or after combined arterial and venous injury. Pain out of proportion and pain on passive stretch are the early signs, with a tense compartment and numbness in the first web space; loss of pulses is late and unreliable. Compartment pressures help when the patient cannot be examined: a perfusion gradient (diastolic pressure minus compartment pressure) under 30 mmHg supports the diagnosis. Treatment is prompt four-compartment fasciotomy, and many surgeons release the compartments at the time of revascularization when the ischemic time has been long.

French measures diameter in thirds of a millimeter, so 1 Fr is about 0.33 mm and 3 Fr is about 1 mm. A catheter is sized by its outer diameter, but a sheath is sized by its inner diameter (the largest device it accepts), so the hole in the artery is roughly 2 Fr larger than the number on the sheath. Wires are sized in inches by diameter: 0.035 is the workhorse, 0.018 and 0.014 are for small vessels and tibials. Balloon and stent diameters and lengths are in millimeters, and catheter and wire lengths in centimeters.

Over the medial third of the femoral head, below the inguinal ligament and above the femoral bifurcation, so the artery can be compressed against bone afterwards. Find the femoral head with fluoroscopy and see the bifurcation and the front wall with ultrasound; the skin crease is unreliable, especially in obese patients. On angiography, a puncture above the lowest curve of the inferior epigastric artery is too high.

• High stick. Enters the external iliac above the ligament, where bleeding cannot be compressed and tracks into the retroperitoneum.
• Low stick. Enters the SFA or profunda, which is smaller and has no bony backstop, so pseudoaneurysm, arteriovenous fistula and thrombosis are more likely.

Retroperitoneal hemorrhage, usually from a high stick above the inguinal ligament or a back-wall puncture. Resuscitate, stop or reverse anticoagulation, send a hemoglobin and a type and crossmatch, and get a CT if the patient is stable enough. Many settle with resuscitation and reversal; ongoing instability goes for endovascular control (a covered stent or balloon tamponade) or open repair. It is occult and can be fatal, so a soft groin should not reassure you. See On call.

• Bentson. A 0.035 starting wire with a long, very floppy tip. The classic first wire through the needle or sheath and up the iliacs, because it is unlikely to raise a dissection.
• Glidewire. A hydrophilic, slippery wire, often with an angled tip, for steering through tortuous vessels, selecting branches and crossing tight stenoses and occlusions. It dissects easily, and it should not be pulled back through a metal access needle, which can shear it.
• Rosen. A 0.035 wire with a tight J tip and a moderately stiff shaft, a workhorse for exchanging and delivering sheaths, balloons and stents with less risk of the tip perforating. Large devices such as an EVAR graft go up a stiffer wire such as an Amplatz or Lunderquist.

The usual sequence is to cross with a steerable wire, then exchange through a catheter for a supportive wire before advancing a device. See Wires.

The SFA bends, twists and is compressed with walking and in the adductor canal. A nitinol self-expanding stent springs back after deformation, whereas a balloon-expandable stent can be permanently crushed or kinked. Balloon-expandable stents are chosen where precise placement and high radial force matter in a vessel that does not flex, such as ostial renal and common iliac lesions. The same logic is why stents are avoided across the common femoral and the popliteal behind the knee when possible.

Carbon dioxide angiography below the diaphragm, since CO2 is neither nephrotoxic nor allergenic. It must not be used above the diaphragm (the cerebral, coronary or thoracic arterial circulation) because gas embolism can cause stroke or myocardial ischemia. Its other limits:

• Lower image quality, especially in small tibial and pedal vessels.
• The gas floats, so non-dependent vessels fill better than dependent ones.
• It needs a closed, dedicated delivery system to keep room air out.
• Gas can become trapped in a large aneurysm sac or the mesenteric vessels and cause ischemia.

Many teams use CO2 for the inflow and a small volume of diluted iodinated contrast for the tibial runoff.

Recognize the risk from the eGFR, then hydrate with isotonic saline before and after unless the patient is volume overloaded. Use the least contrast that answers the question: diluted contrast, planned runs, CO2 below the diaphragm, and duplex or non-contrast imaging to plan beforehand. Avoid nephrotoxins such as NSAIDs, manage metformin per local protocol, and check the creatinine afterwards. N-acetylcysteine and sodium bicarbonate gave no benefit over saline in the PRESERVE trial and are not recommended.

Time, distance and shielding, under the principle of ALARA (as low as reasonably achievable). Minimize fluoroscopy time with low-dose pulsed fluoroscopy and low frame-rate runs. Step back, because scatter falls with the square of the distance. Wear a lead apron, thyroid shield and eye protection, and use the ceiling and table shields. Collimate tightly, keep the image detector close to the patient, limit magnification and steep angles, and stand on the detector side of the C-arm, since scatter is highest on the tube side. See Endovascular.

Type II (retrograde filling of the sac from a lumbar artery or the IMA) is the most common and is usually observed; it is treated if the sac keeps growing, with thresholds that vary (commonly 5 to 10 mm). Types I (a failed seal at an attachment site) and III (component separation or a fabric tear) are high-pressure leaks that re-pressurize the sac and must be treated promptly. Type IV (graft porosity) is seen on the completion angiogram and resolves once anticoagulation wears off. Type V, endotension, is sac growth with no visible leak and needs closer imaging. The table is in Quick reference.

May-Thurner syndrome (iliac vein compression): the left common iliac vein is compressed between the overlying right common iliac artery and the lumbar spine, which is one reason iliofemoral DVT is more common on the left. Anticoagulate. In selected patients with severe symptoms and a low bleeding risk, catheter-directed thrombus removal clears the clot, after which venography and intravascular ultrasound show the compression and a dedicated venous stent treats it. Compression is common on imaging in people without symptoms and is not treated by itself.

Clinical, etiologic (primary, secondary or congenital), anatomic (superficial, deep or perforator) and pathophysiologic (reflux, obstruction or both). The clinical classes are C0 nothing visible, C1 telangiectasias or reticular veins, C2 varicose veins, C3 edema, C4 skin changes, C5 healed ulcer and C6 active ulcer. The 2020 revision split C4 into C4a (pigmentation or eczema), C4b (lipodermatosclerosis or atrophie blanche) and C4c (corona phlebectatica), and added "r" for recurrent varicose veins or ulcers (C2r, C6r). The table is in Quick reference.

Massive iliofemoral DVT that blocks almost all venous outflow from the leg, producing a painful, swollen, blue leg. Phlegmasia alba dolens is the earlier, pale stage. Unrelieved, the venous hypertension raises compartment pressures, compromises arterial inflow and can progress to venous gangrene; an underlying malignancy is common. Start therapeutic heparin immediately, elevate the leg and resuscitate, then arrange urgent thrombus removal (catheter-directed pharmacomechanical thrombectomy or lysis, or open venous thrombectomy), with fasciotomy for compartment syndrome. It threatens both the limb and the patient's life.

The clear indication is acute proximal DVT or PE in a patient who cannot be anticoagulated (active bleeding, recent intracranial hemorrhage, imminent major surgery) or who has a complication that forces anticoagulation to stop. A filter does not treat the clot, so start anticoagulation as soon as it is safe. Adding a filter to anticoagulation did not reduce recurrent PE in PREPIC2, so routine use alongside anticoagulation is not recommended, and apparent failure of anticoagulation should first prompt a check of adherence and dosing. If a retrievable filter goes in, document a retrieval plan and date, because filters left long term cause caval thrombosis, strut penetration and fracture.

Get a duplex first, because superficial vein thrombosis often coexists with DVT and the scan defines the length and the distance from the saphenofemoral junction.

• Short segment, away from the junction. Warm compresses, an NSAID and compression.
• 5 cm or longer. Prophylactic-dose anticoagulation, classically fondaparinux 2.5 mg daily for 45 days.
• Within about 3 cm of the junction. Treated like a DVT with therapeutic anticoagulation, because it can propagate into the common femoral vein. Recommended duration varies by guideline.

Estimate the pretest probability with the Wells score. If DVT is unlikely (Wells under 2), a negative high-sensitivity D-dimer rules it out without imaging. If DVT is likely, or the D-dimer is positive, get a duplex: a whole-leg study, or a proximal compression study repeated in about a week if negative. A non-compressible vein is the key finding. D-dimer is much less useful after surgery and in cancer, pregnancy and old age, because it is so often positive. The score is in Quick reference.

At least three months for any proximal DVT. A DVT provoked by a major transient risk factor such as surgery is treated for three months and then stopped. An unprovoked DVT, or one with a persistent risk factor, is treated for three months and then assessed for extended therapy if the bleeding risk allows. Cancer-associated clot is treated as long as the cancer is active. A DOAC is preferred over warfarin for most patients, but warfarin is preferred in antiphospholipid syndrome. Isolated calf DVT can be anticoagulated or followed with serial duplex for propagation.

Not most patients. In ATTRACT, adding pharmacomechanical catheter-directed thrombolysis to anticoagulation for proximal DVT did not prevent post-thrombotic syndrome overall and increased major bleeding, though it reduced the severity of the syndrome. It is reserved for selected patients: phlegmasia or a threatened limb, and acute (roughly under two weeks) iliofemoral DVT with severe symptoms, good functional status and a low bleeding risk. Femoropopliteal DVT alone is treated with anticoagulation.

Paget-Schroetter syndrome: effort thrombosis of the subclavian and axillary vein from compression in the costoclavicular space (venous thoracic outlet syndrome). Duplex or venography confirms it. Management is anticoagulation, usually early catheter-directed thrombolysis, then decompression of the thoracic outlet by first rib resection, with timing that varies by surgeon and venography afterwards to decide whether the vein needs angioplasty. Stenting the vein before decompression is avoided because the stent gets crushed.

Intra-abdominal hypertension is a sustained intra-abdominal pressure of 12 mmHg or more. Abdominal compartment syndrome is a sustained pressure above 20 mmHg with new organ dysfunction. Pressure is measured through the bladder, supine, at end-expiration, zeroed at the mid-axillary line, after instilling no more than 25 mL of saline. On a vascular service the classic setting is a ruptured AAA repair, open or endovascular, with massive resuscitation and a retroperitoneal hematoma. Watch for a tense abdomen, rising peak airway pressures, falling urine output and hypotension. Sedation, paralysis and gastric and rectal decompression buy little time; the definitive treatment is decompressive laparotomy.

Ischemic colitis, usually of the sigmoid and left colon, from loss of IMA flow on top of poor internal iliac and collateral flow and perioperative hypotension. Any diarrhea in the first days, especially bloody, or a rising lactate, fever, leukocytosis or unexplained acidosis, should prompt a bedside flexible sigmoidoscopy. Mucosal ischemia is managed with bowel rest, fluids, antibiotics and repeat endoscopy; transmural necrosis or peritonitis needs urgent colectomy, usually with an end colostomy. It is more common after rupture than elective repair and can follow EVAR. Transmural necrosis is often lethal, so the threshold to scope is low. See On call.

Treat it as spinal cord ischemia and act within minutes, because it can be reversed. Raise the mean arterial pressure with fluids and vasopressors (commonly to 90 mmHg or higher). Place a lumbar CSF drain if there is none, or lower the drain level, to bring CSF pressure down (often to 10 mmHg or less, within the hourly drainage limit). Transfuse to keep the hemoglobin up, optimize oxygenation and cardiac output, and do frequent neurologic checks. If a drain was recently placed, check coagulation and consider spinal imaging for a hematoma. Every target here is set per local protocol; document the time of onset and every change. See Spinal drains.

Assume an expanding hematoma that threatens the airway. Call for help at once (the senior, anesthesia and the OR), sit the patient up, give oxygen, and assess stridor and work of breathing. If the airway is failing and cannot be secured immediately, open the incision at the bedside, including the platysma closure, to release the hematoma, then go to the OR to find the bleeding. Intubation can be very difficult because of tracheal deviation and laryngeal edema, so the most experienced airway provider should do it. A small, stable hematoma is observed with blood pressure control. See On call.

Cerebral hyperperfusion syndrome. A hemisphere that lost its autoregulation behind a tight stenosis suddenly receives full pressure. It presents with ipsilateral headache, often frontal or behind the eye, then seizures, focal deficits and intracerebral hemorrhage, usually within the first week after CEA or stenting. Risk factors are a high-grade stenosis, poor collateral reserve (such as a contralateral occlusion), recent stroke and perioperative hypertension. Get a head CT to exclude hemorrhage, control blood pressure tightly to the target the team sets, and treat seizures. Prevention is careful blood pressure control after surgery.

Reperfusion releases potassium, acid, myoglobin and inflammatory mediators from damaged muscle. Expect hyperkalemia and acidosis (with a risk of arrhythmia or arrest as flow returns), rhabdomyolysis with pigment kidney injury, compartment syndrome and sometimes lung injury. Check potassium, a blood gas, CK and urine output. Treat hyperkalemia with IV calcium to stabilize the myocardium, insulin with dextrose and an inhaled beta-agonist, bicarbonate for severe acidosis and dialysis if refractory, and give generous IV fluid to keep urine output up. Warn anesthesia before flow is restored.

Heparin-induced thrombocytopenia, an antibody against heparin and platelet factor 4 complexes that activates platelets, so it causes thrombosis rather than bleeding. The typical picture is a fall of more than 50 percent, 5 to 10 days after starting heparin (sooner with heparin exposure in the past few months). Score it with the 4T score. If HIT is likely:

• Stop all heparin, including flushes and heparin-bonded lines.
• Start a non-heparin anticoagulant, such as argatroban or bivalirudin.
• Send the PF4 antibody immunoassay, confirmed with a functional test such as the serotonin-release assay.
• Avoid routine platelet transfusion, do not start warfarin until the platelets recover, and record HIT as an allergy.

The 4T score is in Quick reference.

Cardiac events, especially myocardial infarction, because the vascular patient almost always has coronary disease too. Perioperative MI is often silent, showing up as hypotension, a new arrhythmia, heart failure or simply a rising troponin, so many centers check troponins after major vascular surgery in high-risk patients. Continue beta-blockers in patients already taking them, keep statins and antiplatelets going unless there is a reason not to, and treat a postoperative troponin rise as a reason to optimize cardiac care. Risk scoring is in Quick reference.

The heart, usually atrial fibrillation; mural thrombus after an MI is next.

The common femoral bifurcation.

Pain, pallor, pulselessness, paresthesia, paralysis and poikilothermia. Paresthesia and paralysis are the ominous late signs.

Buttock and thigh claudication, erectile dysfunction and absent femoral pulses, from aortoiliac occlusive disease.

Thromboangiitis obliterans, an inflammatory occlusion of small and medium arteries in young smokers, classically men. The cure is absolute cessation of all tobacco.

Smoking, and smoking cessation.

Proximal subclavian stenosis or occlusion with reversed flow down the vertebral artery, more often on the left. Look for unequal arm pressures, and arm claudication or vertebrobasilar symptoms with arm exercise.

Transient monocular blindness, "a shade coming down", from a retinal artery embolus. The ipsilateral carotid is now symptomatic.

A one-time ultrasound in men 65 to 75 who have ever smoked (USPSTF). The SVS also suggests screening women 65 to 75 who have smoked, and first-degree relatives of patients with an AAA.

Acute mesenteric ischemia until proven otherwise.

Because it lodges a few centimeters beyond the origin, distal to the first jejunal branches. A thrombosis at the origin takes the whole midgut.

Postprandial pain, food fear and weight loss.

Compression of the celiac artery by the median arcuate ligament of the diaphragm. Treat by surgical release, not a stent alone, which gets crushed.

Popliteal. It thromboses and embolizes rather than ruptures, and it is often bilateral and associated with an AAA, so image the other knee and the aorta.

Splenic artery. It can rupture in pregnancy, so it is treated at any size in a woman of childbearing potential.

Massive iliofemoral DVT with a swollen, painful, blue leg. A limb-threatening emergency.

The left common iliac vein compressed by the right common iliac artery.

Effort thrombosis of the subclavian vein in a young, active arm.

Medial malleolus (the gaiter area) versus the toes, heel and pressure points.

Compression versus revascularization. Never compress an ischemic leg; check the ABI first.

A mature fistula by about 6 weeks: flow over 600 mL/min, diameter over 6 mm, depth under 6 mm, and about 6 cm of straight vein to cannulate.

Protamine, roughly 1 mg per 100 units of heparin still active. Give it slowly because of hypotension and anaphylaxis.

Idarucizumab reverses dabigatran. Andexanet alfa or four-factor PCC is used for apixaban and rivaroxaban, depending on local protocol and availability.

About 80 to 100 units per kg IV, with an activated clotting time above roughly 250 seconds before the clamp goes on.