26. Vascular CT

Computed tomographic angiography of the intracranial circulation is the pivotal vascular study of the acute neurological emergency because it converts a clinical syndrome into a mechanistic, treatable lesion within minutes of the noncontrast scan. The governing pathophysiology is abrupt thromboembolic interruption of a large intracranial artery, most often the intracranial internal carotid artery (ICA) terminus or the proximal middle cerebral artery (M1/M2 segments), producing a column of non-opacified vessel distal to the clot. On CTA the finding is a discrete cutoff of the contrast column; on the preceding noncontrast CT the same clot is frequently visible as the $\textbf{hyperdense vessel sign}$, an intraluminal thrombus measuring on the order of $\sim 50$–$80\,\text{HU}$ that exceeds the attenuation of flowing blood and of the contralateral artery, with a vessel Hounsfield ratio above $\sim 1.2$ being a useful quantitative confirmation. The mechanistic value of CTA extends beyond the clot to the $\textbf{collateral circulation}$: leptomeningeal pial vessels retrogradely fill the ischemic territory, and the vigor of that filling—graded on single-phase or, more reliably, multiphase CTA—is an independent determinant of how rapidly the penumbra converts to core. Robust collaterals enlarge the salvageable mismatch that DAWN and DEFUSE 3 exploited for late-window thrombectomy.

The disciplined $\textbf{search pattern}$ proceeds proximal to distal and bilaterally for symmetry: cervical and petrous ICA, cavernous and supraclinoid segments, the ICA terminus, then the M1–M3, A1–A3, and P1–P3 segments, with deliberate interrogation of the basilar apex and the circle of Willis. Each occlusion is characterized by site, clot length (longer thrombi resist intravenous lysis), and downstream collateral grade. The $\textbf{ranked differential}$ for an abrupt cutoff is governed by Bayesian priors: in an older patient with vascular risk factors and atrial fibrillation, cardioembolic or large-artery thromboembolic occlusion dominates; in a younger patient or one with neck trauma or pain, arterial $\textbf{dissection}$ rises sharply and is sought as a tapered or flame-shaped narrowing with an intimal flap or intramural crescent on fat-suppressed sequences; vasospasm is prioritized in the setting of recent subarachnoid hemorrhage; and a non-tapering smooth narrowing with delayed reconstitution suggests intracranial atherosclerotic stenosis, particularly in patients of East Asian, Black, or Hispanic ancestry in whom intracranial atherosclerosis is epidemiologically more prevalent. Beyond occlusive disease, CTA screens for the $\textbf{aneurysm}$ underlying nontraumatic subarachnoid hemorrhage and for the nidus and enlarged feeding arteries and draining veins of an arteriovenous malformation.

The $\textbf{management implications}$ are immediate and trial-defined. Confirmation of an anterior-circulation large-vessel occlusion with favorable imaging triggers mechanical thrombectomy, whose benefit was established across the HERMES pooled analysis and extended into the 6–24 hour window by perfusion- or clinical-mismatch selection. CTA additionally maps the access anatomy—aortic arch type, cervical tortuosity, tandem cervical ICA disease—that determines procedural feasibility. The $\textbf{failure modes}$ are specific and consequential. Technically, suboptimal bolus timing renders a patent distal vessel falsely occluded, venous-phase contamination obscures arterial detail, and motion or beam-hardening from dense dental amalgam degrades the skull base. Cognitively, $\textbf{satisfaction of search}$ after identifying an M1 occlusion causes the reader to overlook a tandem cervical ICA lesion or a contralateral aneurysm, while $\textbf{anchoring}$ on a presumed embolus delays recognition of an underlying dissection in a young patient—an error with direct therapeutic consequence because the secondary-prevention strategy differs.

Extracranial carotid atherosclerotic disease is the proximate cause of roughly one in five ischemic strokes, and its imaging is fundamentally a problem of quantifying a luminal stenosis and characterizing the plaque that generates emboli. The pathophysiology is progressive intimal atheroma at the carotid bifurcation, where flow separation and low oscillatory wall shear stress favor lipid deposition; the lesion threatens the brain by two mechanisms—hemodynamic flow limitation when the stenosis becomes critical, and, far more commonly, $\textbf{artery-to-artery thromboembolism}$ from a ruptured or ulcerated plaque. CTA depicts the residual contrast-filled lumen with sub-millimeter isotropic resolution, and stenosis is quantified by the $\textbf{NASCET method}$: the ratio of the narrowest residual luminal diameter to the diameter of the normal distal cervical ICA, expressed as $\%\,\text{stenosis} = \left(1 - \dfrac{D_{\text{stenosis}}}{D_{\text{distal-normal}}}\right)\times 100$. This denominator convention is essential and distinguishes NASCET from the ECST method, which used the estimated original bulb diameter and therefore yields systematically higher percentages for the same anatomy.

The $\textbf{CT signature}$ extends to plaque morphology, a domain where CT is uniquely informative. Calcified plaque is conspicuous but stable; the higher-risk features are a large lipid-rich necrotic core (low-attenuation plaque, frequently $< 30$–$60\,\text{HU}$), surface ulceration (a contrast-filled outpouching extending into the plaque beyond the expected luminal contour), and a thin or ruptured fibrous cap. The companion modality, Doppler ultrasound, quantifies stenosis hemodynamically; the $\textbf{Society of Radiologists in Ultrasound (SRU)}$ consensus thresholds anchor the velocity criteria, with a peak systolic velocity (PSV) $\geq 230\,\text{cm/s}$ together with an ICA/CCA PSV ratio $\geq 4$ and end-diastolic velocity $\geq 100\,\text{cm/s}$ defining $\geq 70\%$ stenosis, while PSV $125$–$230\,\text{cm/s}$ corresponds to the $50$–$69\%$ band. The $\textbf{search pattern}$ examines the common carotid, the bifurcation, and the proximal and distal ICA for stenosis grade, plaque character, ulceration, tandem intracranial disease, and the contralateral vessel, and specifically evaluates for the $\textbf{string sign}$—a trickle of contrast through a near-occlusion that must not be mistaken for complete occlusion, because the two diagnoses diverge in management.

The $\textbf{ranked differential}$ for carotid narrowing is led by atherosclerosis in older patients with vascular risk factors; in younger patients or after trauma, $\textbf{dissection}$ predominates and shows a tapered narrowing with an eccentric mural hematoma; fibromuscular dysplasia produces a characteristic mid-cervical 'string of beads'; radiation arteriopathy is suggested by long smooth narrowing within a prior radiation port; and vasculitis (Takayasu, giant cell) by concentric wall thickening and enhancement. The $\textbf{management}$ threshold is trial-defined: NASCET established the benefit of carotid endarterectomy for symptomatic stenosis $\geq 70\%$ and a more modest benefit for $50$–$69\%$, while CREST demonstrated comparable composite outcomes for carotid artery stenting and endarterectomy, with periprocedural stroke commoner after stenting and myocardial infarction commoner after surgery, and with patient age favoring endarterectomy in older patients. The $\textbf{failure modes}$ are dominated by densely calcified plaque, whose $\textbf{blooming}$ artifact spuriously narrows the apparent lumen and overestimates stenosis—a pitfall mitigated by wide windowing, multiplanar review, or dual-energy/photon-counting acquisition that suppresses blooming. The principal cognitive error is misclassifying a near-occlusion string sign as a complete occlusion, thereby withdrawing a patient from beneficial revascularization.

The posterior circulation supplies the brainstem, cerebellum, thalami, and occipital cortex, and its CT angiographic evaluation is distinguished by both higher diagnostic difficulty and higher stakes than the anterior circulation. The vertebral arteries arise from the subclavian arteries, ascend through the transverse foramina from C6 to C1, traverse a mobile atlanto-axial (V3) segment, and pierce the dura to join as the basilar artery. The pathophysiology of posterior-circulation ischemia is heterogeneous: $\textbf{vertebral artery dissection}$ is disproportionately a disease of younger patients and follows neck trauma, chiropractic manipulation, or even trivial mechanical strain, predominating at the mobile V3 segment; $\textbf{atherosclerotic stenosis}$ clusters at the vertebral origin and the vertebrobasilar junction; and $\textbf{embolism}$—cardiac or artery-to-artery—lodges at the basilar apex. Basilar occlusion is the catastrophic endpoint, carrying a historically dismal prognosis because it threatens the reticular activating system and the entire brainstem.

The $\textbf{CT signature}$ of acute basilar thrombosis on noncontrast CT is the $\textbf{hyperdense basilar artery sign}$, an intraluminal clot of $\sim 50$–$70\,\text{HU}$ standing out against the hypodense pons and the surrounding cerebrospinal fluid; on CTA the basilar contrast column terminates abruptly. Dissection on CTA manifests as a tapered or flame-shaped vertebral narrowing, an intimal flap, a $\textbf{pseudoaneurysm}$ (a focal saccular outpouching), or an eccentric mural hematoma that on cross-section narrows the true lumen; the diagnosis is frequently more conspicuous on fat-suppressed T1 MRI, where the crescentic methemoglobin signal is unmistakable, so a negative CTA in a high-suspicion patient should prompt MRI. The $\textbf{search pattern}$ must be deliberate and bilateral because vertebral hypoplasia is a common normal variant—one congenitally small or terminating-in-PICA vertebral artery is not an occlusion—and the reader traces both vertebrals from origin to confluence, the full basilar trunk, the posterior inferior, anterior inferior, and superior cerebellar arteries, and the posterior cerebral arteries, while interrogating the brainstem on noncontrast images for established hypodensity.

The $\textbf{ranked differential}$ for a posterior-circulation narrowing is led by atherosclerosis in older vasculopaths and by dissection in younger patients or after mechanical neck stress; vertebral hypoplasia and a dominant-vertebral configuration are the leading benign mimics; vasospasm follows subarachnoid hemorrhage; and the rotational compression of $\textbf{bow hunter's syndrome}$ produces dynamic vertebral occlusion on head turning. The $\textbf{management}$ stakes are high: acute basilar occlusion is now treated with endovascular thrombectomy on the strength of the ATTENTION and BAOCHE trials, which demonstrated functional benefit despite the technical difficulty, and dissection is managed with antithrombotic therapy (the choice of antiplatelet versus anticoagulation guided by the cervical artery dissection literature) with endovascular intervention reserved for enlarging pseudoaneurysm or recurrent ischemia. The $\textbf{failure modes}$ are particularly treacherous here: $\textbf{posterior-fossa beam-hardening}$ (the Hounsfield interpetrous dark band) obscures the brainstem on noncontrast CT and hides early infarction; the small caliber and tortuosity of the vessels make subtle dissection easy to miss; and the dominant cognitive trap is dismissing a true vertebral occlusion as benign hypoplasia, or anchoring on a 'normal' anterior circulation while a devastating basilar thrombus declares itself only as a faintly hyperdense vessel and a depressed level of consciousness out of proportion to focal signs.

The aorta presents two distinct CT problems—the acute aortic syndrome and the chronic aneurysm—both diagnosed by ECG-gated or fast non-gated CT angiography, which is the standard of care for its speed, near-complete anatomic coverage, and reproducibility. The $\textbf{acute aortic syndromes}$ share a final common pathway of medial failure. In classic $\textbf{dissection}$, blood enters the media through an intimal tear and propagates a false lumen separated from the true lumen by an intimointimal flap; on CTA the flap is a thin curvilinear filling defect, and interpretation turns on identifying the true and false lumina and the proximal and distal extent. The decisive classification is the $\textbf{Stanford}$ scheme: type A involves the ascending aorta and is a surgical emergency because of the risk of pericardial tamponade, aortic-valve incompetence, and coronary or arch-vessel malperfusion, whereas type B begins distal to the left subclavian artery and—when uncomplicated—is managed medically with aggressive anti-impulse therapy, reserving thoracic endovascular aortic repair (TEVAR) for complications. The $\textbf{DeBakey}$ scheme refines anatomy (type I: ascending, arch, and descending; type II: ascending only; type III: descending only). Identifying the $\textbf{true lumen}$ is operationally essential because the stent-graft and the dominant outflow must address it; the true lumen is usually smaller, continuous with the undissected aorta, and may show the $\textbf{beak sign}$ at the acute angle of the flap, while the false lumen is often larger, opacifies later, and may contain the $\textbf{cobweb sign}$ of residual incompletely sheared media.

The other two syndromes share the threat with different signatures. $\textbf{Intramural hematoma}$ is a crescentic, non-enhancing high-attenuation thickening ($> 5\,\text{mm}$, frequently $60$–$70+\,\text{HU}$ on noncontrast imaging) within the wall, representing vasa vasorum hemorrhage without a demonstrable flap; the noncontrast acquisition is indispensable because contrast can mask the intrinsic hyperattenuation, and management follows the same ascending-versus-descending logic. The $\textbf{penetrating atherosclerotic ulcer}$ is a contrast-filled outpouching extending beyond the intimal contour through an ulcerated plaque, often with adjacent intramural hematoma, signaling high rupture risk when deep, wide, or enlarging. The $\textbf{search pattern}$ extends beyond the flap to its consequences: pericardial and mediastinal hemorrhage, periaortic and pleural blood signaling contained rupture, and branch-vessel $\textbf{malperfusion}$ of the coronary, arch, visceral, renal, or iliac origins—a major source of mortality recognized when the dissection compromises an ostium or when an organ fails to enhance. For the chronic $\textbf{aneurysm}$, CT measures the maximal orthogonal diameter on double-oblique reformats; per the 2024 ESVS and the 2022 ACC/AHA guidance, elective repair of an infrarenal abdominal aortic aneurysm is generally indicated at $\geq 5.5\,\text{cm}$ in men and $\geq 5.0\,\text{cm}$ in women, or with rapid growth ($> 0.5\,\text{cm}$ in six months) or symptoms, and ruptured or impending-rupture signs (the high-attenuation crescent of mural-thrombus hemorrhage, the draped-aorta sign, retroperitoneal hematoma) demand emergent treatment.

The $\textbf{Bayesian}$ frame operates at triage: tearing interscapular pain, a pulse deficit, mediastinal widening, or a markedly elevated D-dimer raise the pretest probability and justify immediate CTA, with the aortic dissection detection risk score formalizing stratification. The $\textbf{failure modes}$ are notorious. $\textbf{Cardiac-motion artifact}$ at the aortic root produces a curvilinear double contour mimicking an ascending flap—the single most common false positive—resolved by ECG gating or by recognizing its motion-blur character; streak artifact from dense contrast in the superior vena cava, pulsation, and beam-hardening likewise generate pseudoflaps. Conversely, the true flap of a slow-flow or thrombosed false lumen can be subtle, and the gravest cognitive errors are anchoring on a benign mimic to dismiss a real type A dissection and satisfaction of search, in which the flap is found but a critical malperfusion or contained rupture that dictates the operative plan is overlooked.

Lower-extremity peripheral arterial disease (PAD) is the systemic atherosclerotic burden made visible in the limb, and CT angiography from the infrarenal aorta to the pedal arch has become a workhorse for revascularization planning. The pathophysiology is segmental atherosclerotic stenosis and occlusion of the aortoiliac, femoropopliteal, and infrapopliteal (tibial) levels, with the hemodynamic consequence determined by both the severity of the lesion and the adequacy of the $\textbf{collateral}$ network that reconstitutes flow distal to an occlusion. The clinical spectrum is graded by the $\textbf{Rutherford}$ classification (categories 0–6) and the parallel Fontaine stages, ranging from asymptomatic disease through intermittent claudication to the limb-threatening categories of rest pain (Rutherford 4) and tissue loss (Rutherford 5–6); the latter two constitute $\textbf{chronic limb-threatening ischemia (CLTI)}$, the modern term that supplants 'critical limb ischemia' and is staged for amputation risk by the $\textbf{WIfI}$ system (Wound, Ischemia, foot Infection) endorsed by the Global Vascular Guidelines.

The $\textbf{CT signature}$ is read level by level. At each segment the reader records the presence and length of stenosis or occlusion, the burden and distribution of calcification, and the level at which a patent vessel reconstitutes via collaterals—because the length of an occlusion and the quality of the distal target (the 'runoff') determine whether an endovascular or surgical bypass strategy will succeed. Hemodynamically significant stenosis is generally taken as luminal narrowing $\geq 50\%$ by diameter, which corresponds to a roughly $75\%$ cross-sectional area reduction and a measurable pressure gradient. The $\textbf{search pattern}$ is systematic and bilateral: infrarenal aorta and the iliac arteries, common and deep and superficial femoral arteries, the popliteal artery and its trifurcation, and the anterior tibial, posterior tibial, and peroneal arteries to the ankle and into the pedal arch, with explicit notation of inline flow to the foot, which is the anatomic substrate of wound healing. The $\textbf{ranked differential}$ for arterial narrowing is dominated by atherosclerosis in the typical older diabetic or smoking patient; in a young patient with calf claudication, $\textbf{popliteal artery entrapment}$ or $\textbf{cystic adventitial disease}$ rises in probability; embolic occlusion produces an abrupt cutoff with a meniscus and minimal collateral; thromboangiitis obliterans (Buerger disease) affects distal vessels in young smokers with a 'corkscrew' collateral pattern; and acute limb ischemia from in-situ thrombosis or embolism is a surgical emergency distinguished by its abruptness and paucity of collaterals.

The $\textbf{management}$ framework follows the 2024 ACC/AHA PAD guideline and the GVG: claudication is treated first with structured exercise, statins, antiplatelet therapy, and smoking cessation, with revascularization for lifestyle-limiting symptoms; CLTI mandates prompt revascularization to preserve the limb, with the anatomic pattern (focal vs. long-segment, good vs. poor runoff) and patient risk steering the choice between endovascular therapy and surgical bypass. The $\textbf{failure modes}$ center on calcium: dense circumferential $\textbf{tibial calcification}$ in diabetic and renal patients blooms and obscures the residual lumen, the single most important cause of overestimated stenosis on CTA, mitigated by wide windowing, dual-energy or photon-counting calcium subtraction, or recourse to alternative imaging. $\textbf{Bolus mistiming}$ in a limb with slow inflow can fail to opacify a patent distal vessel, fabricating an occlusion, and asymmetric runoff means the scan may outrun the contrast in the more diseased leg. The principal cognitive error is satisfaction of search after the index proximal lesion, with failure to document the distal target whose patency actually determines reconstructive feasibility.

The venous compartment generates several of CT's highest-volume and highest-acuity diagnoses, unified by the pathophysiology of thrombosis and its hemodynamic sequelae. $\textbf{Pulmonary embolism (PE)}$ is the dominant indication: a thrombus, usually embolized from the deep veins of the legs or pelvis, lodges in the pulmonary arterial tree and is depicted on CT pulmonary angiography (CTPA) as a low-attenuation intraluminal filling defect, either occlusive or producing the $\textbf{polo-mint}$ sign (a central defect surrounded by contrast on a cross-section) or the $\textbf{railway-track}$ sign (a longitudinal defect) acutely, in contrast to the eccentric, mural, calcified, or web-like defects of chronic organized thrombus. The clinically decisive extension of the search is to $\textbf{right-heart strain}$, the proximate cause of death in PE: a right-ventricle-to-left-ventricle short-axis diameter ratio $> 1.0$ (and especially $\geq 1.5$), straightening or leftward bowing of the interventricular septum, and reflux of contrast into the inferior vena cava and hepatic veins together stratify a hemodynamically significant embolism. The 2019 ESC framework integrates these CT signs with biomarkers and clinical scores to classify PE as low-risk, intermediate-risk, or high-risk, the last warranting reperfusion (systemic thrombolysis or catheter-directed therapy) rather than anticoagulation alone.

$\textbf{Deep vein thrombosis (DVT)}$ is imaged on CT as an expanded, non-opacified vein with a low-attenuation intraluminal filling defect and surrounding mural enhancement and perivenous stranding when acute; CT venography of the pelvis and thighs complements CTPA when leg symptoms accompany suspected PE. Clot age is inferred from morphology—an acute thrombus expands the vein and is of soft-tissue attenuation, whereas a chronic clot retracts the vein, may calcify, and recanalizes. A specific and frequently overlooked entity is $\textbf{May-Thurner syndrome}$, in which the right common iliac artery compresses the left common iliac vein against the lumbar spine, producing left-leg DVT in young patients; CT shows the focal venous compression with prominent pelvic and lumbar collaterals, and its recognition changes management toward venous stenting. $\textbf{Cerebral venous thrombosis (CVT)}$ is the neurological counterpart: on noncontrast CT the thrombosed dural sinus or cortical vein is hyperdense (the dense-vein or cord sign), and on CT venography the filling defect within an opacified sinus produces the $\textbf{empty delta sign}$ in the superior sagittal sinus; the 2024 AHA scientific statement codifies the diagnostic pathway and anticoagulation even in the presence of venous hemorrhagic infarction.

The $\textbf{search pattern}$ in CTPA proceeds from the main and lobar arteries—where a missed central embolus is indefensible—to the segmental and subsegmental branches, then deliberately to the cardiac chambers for strain and to the lung bases and pleura for infarction (the peripheral wedge-shaped $\textbf{Hampton hump}$). The $\textbf{ranked differential}$ and mimics are dominated by the technical: a $\textbf{flow-related filling defect}$ from transient interruption of the contrast bolus by unopacified blood (often from a deep inspiration drawing IVC blood into the right atrium) is the classic PE mimic, distinguished by its ill-defined margins, location at confluences, and resolution on repeat or on recognizing the suboptimal main-pulmonary-artery opacification. The $\textbf{failure modes}$ thus center on $\textbf{bolus mistiming}$ and respiratory-motion artifact at the lung bases, which degrade exactly the segmental vessels most often harboring small emboli; beam-hardening from dense contrast in the superior vena cava simulates defects in the adjacent right pulmonary artery. Cognitively, anchoring on a single conspicuous embolus invites satisfaction of search for the equally important assessment of clot burden and right-heart strain that drives the risk-stratified anticoagulation and reperfusion decisions of the 2021 CHEST guidance.

Mesenteric ischemia is among the most lethal abdominal vascular emergencies, with a mortality that rises steeply with each hour of delayed diagnosis, and multiphase CT angiography is the decisive test. The pathophysiology partitions into mechanistically distinct categories that the CT reader must separate because they diverge in treatment. $\textbf{Acute mesenteric ischemia (AMI)}$ is most often $\textbf{arterial embolic}$—a cardiac embolus lodging in the superior mesenteric artery (SMA), characteristically several centimeters beyond the origin and sparing the proximal jejunal and middle colic branches; less commonly it is $\textbf{arterial thrombotic}$, superimposed on pre-existing ostial atherosclerosis and therefore occluding at the SMA origin; $\textbf{venous}$, from superior mesenteric vein thrombosis in hypercoagulable or portal-hypertensive patients; or $\textbf{nonocclusive (NOMI)}$, a low-flow vasospastic state in critically ill, hypotensive, or vasopressor-dependent patients in whom the named vessels are patent but the bowel is hypoperfused. $\textbf{Chronic mesenteric ischemia}$ reflects atherosclerotic stenosis of two or more of the three mesenteric vessels (celiac, SMA, inferior mesenteric artery) with postprandial 'intestinal angina,' weight loss, and food fear.

The $\textbf{CT signature}$ is acquired with a properly timed multiphase protocol—a noncontrast phase to detect intrinsic hyperdensity, a CT-arteriographic phase to demonstrate the arterial occlusion, and a portal-venous phase to assess venous patency and bowel-wall enhancement. The arterial findings are the intraluminal embolic filling defect or the ostial occlusion; the venous finding is an expanded SMV with a central filling defect. The bowel findings are the crux and evolve with severity: early reversible ischemia shows bowel-wall thickening and submucosal edema, whereas the ominous signs of transmural infarction are $\textbf{absent or diminished mural enhancement}$ (the most specific sign of nonviable bowel), $\textbf{pneumatosis intestinalis}$ (gas dissecting the bowel wall), and $\textbf{portomesenteric venous gas}$ (branching lucencies extending to the hepatic periphery, distinct from the central pneumobilia of biliary origin). Paradoxically, in NOMI the bowel wall may appear thin and paper-like rather than thickened, with poor enhancement and segmental spasm. The $\textbf{search pattern}$ traces the celiac, SMA, and IMA from origin to distal branches, evaluates the mesenteric and portal venous return, scrutinizes every bowel segment for wall thickness and the presence or absence of enhancement, and surveys for pneumatosis, portal venous gas, ascites, and mesenteric stranding.

The $\textbf{ranked differential}$ is governed by clinical priors codified in the WSES guidelines: in a patient with atrial fibrillation or recent myocardial infarction, SMA embolism dominates; with diffuse atherosclerosis and prior intestinal angina, SMA-origin thrombosis; with hypercoagulability, portal hypertension, or recent abdominal surgery, venous thrombosis; and in the shocked ICU patient on pressors, NOMI. The principal $\textbf{mimics}$ are benign $\textbf{pneumatosis}$ (a chronic, asymptomatic finding in COPD or post-transplant patients without ischemia) and the bowel-wall thickening of infectious or inflammatory enteritis. The $\textbf{management}$ imperative is speed: occlusive AMI demands urgent revascularization (surgical embolectomy or endovascular thrombectomy/thrombolysis) and resection of frankly infarcted bowel, NOMI is treated by reversing the low-flow state and intra-arterial vasodilators, and chronic mesenteric ischemia is treated electively by stenting or bypass; the presence of pneumatosis with portal venous gas and peritonitis mandates immediate surgical involvement. The $\textbf{failure modes}$ are unforgiving. Technically, a single portal-venous acquisition without an arterial phase can miss the embolus, and respiratory motion or poor opacification degrades the SMA. The dominant cognitive trap is being reassured by 'normal-looking' bowel calibre in NOMI or by the absence of dramatic findings early in embolic ischemia, where the only clue may be subtle decreased enhancement of a bowel segment against a backdrop of pain out of proportion to examination—the classic clinical signature that should lower the threshold for diagnosing this time-critical disease.