Vascular Surgery
Aneurysms, dead limbs, and gut angina - the vascular emergencies boards test
Abdominal aortic aneurysm
Definition and risk. An AAA is an aorta ≥3 cm in diameter; most are infrarenal and atherosclerotic. Smoking is the strongest risk factor, followed by male sex, age, and family history. Rupture risk tracks diameter and expansion rate: by Laplace's law, wall tension rises with radius, so larger aneurysms are more dangerous.
Screening. The USPSTF recommends a one-time abdominal ultrasound for men 65–75 who have ever smoked. Screening can be offered selectively to never-smoking men in that age range; routine screening of never-smoking women is not recommended.
Surveillance and elective repair. Repeat ultrasound every 2–3 years for 3.0–3.9 cm and every 6–12 months for 4.0–5.4 cm, with smoking cessation and cardiovascular risk control in the meantime. Repair when the aneurysm reaches ≥5.5 cm, expands rapidly, or becomes symptomatic (tender, or causing back or abdominal pain). Options are endovascular repair (EVAR) or open repair; EVAR has lower perioperative mortality but needs lifelong imaging surveillance for endoleak.
Ruptured AAA. The classic triad is hypotension, sudden severe back or flank pain, and a pulsatile abdominal mass, often with syncope. Overall mortality of rupture is about 80–90%.
- Recognize the triadHypotension, back or flank pain, pulsatile mass in an older smoker.
- UnstableStraight to the operating room without imaging; permissive hypotension until proximal control.
- StableCT angiography first to confirm and plan.
- RepairOpen or EVAR.
Bloody diarrhea after aortic repair suggests ischemic colitis of the sigmoid from loss of inferior mesenteric artery flow. GI bleeding months to years after an aortic graft is an aortoenteric fistula (usually to the duodenum) until proven otherwise.
Peripheral arterial disease
Claudication. Intermittent claudication is reproducible cramping leg pain with walking, relieved by rest within minutes. The pain sits one level below the disease: femoropopliteal disease causes calf pain. Aortoiliac occlusion produces Leriche syndrome: buttock and thigh claudication, erectile dysfunction, and absent femoral pulses. Lumbar spinal stenosis mimics it (pseudoclaudication) but is brought on by standing as well as walking, eases with sitting or leaning forward, and leaves pulses intact.
Ankle-brachial index. ABI = ankle systolic pressure ÷ the higher brachial systolic pressure. It is the first-line noninvasive test.
| ABI | Meaning | Implication |
|---|---|---|
| 1.0–1.4 | Normal | PAD unlikely at rest |
| ≤0.90 | Diagnoses PAD | Risk-factor therapy; symptom-guided treatment |
| <0.40 | Critical or severe ischemia | Evaluate for revascularization |
| >1.40 | Noncompressible, calcified vessels (diabetes, CKD) | Unreliable; use a toe-brachial index |
Management. First-line is supervised exercise plus risk-factor control: smoking cessation, a high-intensity statin, an antiplatelet (aspirin or clopidogrel), and control of blood pressure and diabetes. Cilostazol, a PDE3 inhibitor, improves walking distance but is contraindicated in any degree of heart failure because PDE3 inhibitors raise mortality in HF. Revascularization (endovascular or bypass) is reserved for lifestyle-limiting claudication despite this or for critical limb ischemia: rest pain (burning forefoot pain at night, eased by hanging the foot off the bed), nonhealing ulcers, or gangrene.
Acute limb ischemia
The 6 Ps. Pain, Pallor, Pulselessness, Paresthesia, Paralysis, and Poikilothermia (a cold limb). Sensory loss and weakness mean nerve and muscle are already ischemic and the limb is immediately threatened.
| Feature | Embolism | Thrombosis |
|---|---|---|
| Source | Cardiac, classically atrial fibrillation | Chronic atherosclerotic plaque |
| Onset | Sudden, severe | More gradual |
| History | No prior claudication; normal contralateral limb | Prior claudication; bilateral PAD |
| Collaterals | None | Present, partly compensating |
| Site | Lodges at arterial bifurcations | At the preexisting stenosis |
| Usual fix | Fogarty balloon embolectomy | Catheter-directed thrombolysis or bypass |
Management. Give IV unfractionated heparin at once to stop clot propagation, then revascularize (surgical embolectomy, catheter-directed thrombolysis, or bypass) as guided by limb viability (Rutherford class). The window is about 4–6 hours. A limb with profound sensory loss and paralysis that is no longer salvageable is amputated. Afterward, look for the embolic source (ECG, echocardiogram) and anticoagulate long term when atrial fibrillation is the cause.
Reperfusion can cause compartment syndrome (pain on passive stretch; treat with fasciotomy) and release potassium, acid, and myoglobin from ischemic muscle, causing hyperkalemia and renal injury.
Carotid stenosis
Presentation. Carotid plaque embolizes to cause TIA, stroke, or amaurosis fugax (transient monocular blindness, like a shade coming down over one eye). A bruit correlates poorly with severity; carotid duplex ultrasound is the initial test.
- Symptomatic 70–99%: carotid endarterectomy (CEA) plus medical therapy, ideally within 2 weeks of the event; NASCET established this benefit.
- Symptomatic 50–69%: CEA in selected patients.
- Asymptomatic ≥60–70%: CEA if surgical risk is low and life expectancy is >5 years.
- 100% (complete) occlusion: never revascularized.
Around the operation. Every patient gets an antiplatelet, a statin, and risk-factor control. Carotid stenting is an alternative for high surgical risk (prior neck radiation or surgery). CEA complications include stroke, MI, cerebral hyperperfusion, and cranial nerve injury (hypoglossal: tongue deviates toward the injured side; recurrent laryngeal: hoarseness).
Mesenteric ischemia
| Feature | Acute mesenteric ischemia | Chronic mesenteric ischemia | Ischemic colitis |
|---|---|---|---|
| Cause | SMA embolus (atrial fibrillation) is classic | Atherosclerosis of ≥2 mesenteric arteries | Hypoperfusion of watershed zones: splenic flexure, rectosigmoid |
| Picture | Sudden severe pain out of proportion to a soft, benign exam | Postprandial pain, food fear, weight loss (intestinal angina) | Elderly patient with crampy pain and bloody diarrhea |
| Diagnosis | CT angiography | CT angiography | CT, then colonoscopy |
| Treatment | Heparin, embolectomy or revascularization, resection of necrotic bowel | Elective revascularization: angioplasty/stent or bypass | Usually supportive (bowel rest, fluids); surgery if gangrene or peritonitis |
Rising lactate and metabolic acidosis are late, ominous signs of bowel that has already infarcted. Do not wait for them; a normal early lactate does not exclude acute mesenteric ischemia.
Other acute causes. SMA thrombosis on ostial plaque (often after a history of intestinal angina), nonocclusive ischemia in low-flow states (shock, vasopressors, digoxin), and mesenteric venous thrombosis in hypercoagulable patients (treated with anticoagulation). A second-look operation is often planned to reassess bowel viability.
Deep vein thrombosis
Presentation. Virchow triad (stasis, endothelial injury, hypercoagulability) underlies DVT, which presents with unilateral leg swelling, pain, and warmth.
- Wells scoreEstimate pretest probability.
- Low probabilityCheck D-dimer; a negative result excludes DVT.
- Positive D-dimer or high probabilityCompression duplex ultrasound confirms the diagnosis.
Treatment. A DOAC (rivaroxaban or apixaban) is preferred; the alternative is LMWH bridged to warfarin, overlapping until the INR is therapeutic. Treat provoked DVT for 3 months and consider indefinite therapy for unprovoked or recurrent DVT. Cancer-associated DVT is treated with a DOAC or LMWH. An IVC filter is used only when anticoagulation is contraindicated, such as active bleeding. Complications are pulmonary embolism and post-thrombotic syndrome.