Diagnostic Radiology & Bedside POCUS Master Atlas: CXR, Neuro CT/MRI, Abdominal CT & Sonography

Because the MRI scanner maintains a powerful static magnetic field (1.5 to 3.0 Tesla) and pulsed radiofrequency gradients, ferromagnetic implants can undergo catastrophic torque, dislodgement, or thermal heating. Absolute contraindications to MRI include ferromagnetic intracranial aneurysm clips, metallic intraocular foreign bodies (sheet metal workers must undergo orbital plain radiographs or non-contrast CT screening prior to MRI), cochlear implants, non-MRI-conditional cardiac pacemakers or implantable cardioverter-defibrillators, and retained ferromagnetic shrapnel near vital neurovascular structures. Conversely, most modern orthopedic titanium prostheses, sternal wires, and coronary stents are safe for MRI. Gadolinium-based intravenous MRI contrast agents are chelates that shorten T1 relaxation times wherever the blood-brain barrier is disrupted or tissue vascularity is increased. In patients with severe renal insufficiency (AKI or CKD stage 4/5 with eGFR less than 30 mL/min/1.73m2, especially dialysis patients), dissociation of free gadolinium ions from older linear chelates triggers Nephrogenic Systemic Fibrosis (NSF)—a progressive, debilitating fibrosing disorder starring woody induration, brawny hyperpigmentation, and flexion contractures of the skin and extremities along with visceral organ fibrosis, for which there is no curative therapy.

During pregnancy, non-ionizing modalities—specifically ultrasonography and non-contrast MRI (without gadolinium, as gadolinium crosses the placenta and is excreted into amniotic fluid)—are always preferred as first-line diagnostic studies. For example, suspected appendicitis in a pregnant patient is evaluated initially with graded-compression abdominal ultrasound followed by non-contrast abdominal/pelvic MRI if ultrasound is non-diagnostic. However, medically necessary maternal diagnostic imaging should never be withheld out of fear of fetal radiation when a life-threatening maternal emergency (such as pulmonary embolism or major trauma) is suspected. Fetal deterministic radiation effects (such as microcephaly, growth restriction, or intellectual disability, maximally sensitive at 8-15 weeks gestation) require a cumulative threshold dose exceeding 50-100 mGy (5-10 rad). A maternal chest radiograph with abdominal shielding delivers less than 0.01 mGy to the fetus, and both ventilation-perfusion (V/Q) scanning and CT pulmonary angiography (CTPA) deliver well below 5 mGy. In a pregnant patient with suspected pulmonary embolism, duplex compression ultrasonography of the lower extremities is performed first if DVT symptoms exist; if negative or if only chest symptoms exist, a chest radiograph is obtained: if the CXR is normal, a V/Q scan is preferred (lower maternal breast radiation dose), whereas if the CXR is abnormal, CTPA is performed.

Cardiogenic pulmonary edema progresses sequentially on chest radiography as pulmonary capillary wedge pressure (PCWP) rises: at PCWP 13-18 mmHg, upper lobe pulmonary venous cephalization (redistribution of blood flow to apical vessels) appears; at PCWP 18-25 mmHg, interstitial edema manifests as peribronchial cuffing and Kerley B lines (short 1-2 cm horizontal lines perpendicular to the lateral pleural surface at the lung bases representing thickened interlobular septa); and at PCWP greater than 25 mmHg, alveolar flooding produces bilateral perihilar bat-wing (butterfly) airspace opacities accompanied by cardiomegaly (cardiothoracic ratio greater than 0.5 on PA film) and bilateral pleural effusions. In contrast, Acute Respiratory Distress Syndrome (ARDS, non-cardiogenic pulmonary edema) presents with bilateral diffuse alveolar infiltrates without cardiomegaly, Kerley B lines, or vascular pedicle widening. On high-resolution chest CT (HRCT), distinct parenchymal patterns narrow the differential diagnosis: Tree-in-bud opacities (centrilobular nodules connected to linear branching structures) indicate endobronchiolar mucus impaction characteristic of active endobronchial tuberculosis, nontuberculous mycobacteria (Mycobacterium avium complex), or aspiration bronchiolitis; Basal and subpleural honeycombing with traction bronchiectasis defines the Usual Interstitial Pneumonia (UIP) pattern of idiopathic pulmonary fibrosis; and Halo sign (ground-glass attenuation surrounding a dense pulmonary nodule, representing alveolar hemorrhage around vascular invasion) is classic for angioinvasive pulmonary aspergillosis in neutropenic patients.

In acute aortic syndrome (sudden tearing chest pain radiating to the interscapular back), the screening chest radiograph reveals a widened mediastinum (greater than 8 cm at the aortic arch on AP view), obliteration of the aortic knob, right-sided tracheal deviation, depression of the left mainstem bronchus, or an apical pleural cap (hemothorax), though up to 20% of patients have a normal CXR. In hemodynamically stable patients with adequate renal function, ECG-gated CT angiography (CTA) of the chest, abdomen, and pelvis is the definitive modality of choice, demonstrating an intimal dissection flap separating a true lumen from a false lumen. Stanford Type A dissections involve the ascending aorta (regardless of distal extension) and mandate emergent open surgical repair to prevent fatal pericardial tamponade, acute aortic regurgitation, or right coronary artery occlusion, whereas uncomplicated Stanford Type B dissections are restricted to the descending aorta distal to the left subclavian artery and are managed medically with intravenous beta-blockade (esmolol or labetalol to target heart rate less than 60 bpm and systolic BP 100-120 mmHg) followed by vasodilators (nicardipine or nitroprusside). In acute pulmonary embolism, CXR is most commonly normal (or shows sinus tachycardia and atelectasis), while classic eponymous signs—Westermark sign (focal oligemia distal to an occluded pulmonary artery) and Hampton hump (a peripheral wedge-shaped pleural-based consolidation representing pulmonary infarction)—are specific but rare; CTA provides definitive diagnosis by visualizing an intraluminal arterial filling defect.

In the first 3-6 hours of an acute ischemic stroke, non-contrast head CT is frequently normal (its primary urgency is excluding hemorrhage prior to intravenous alteplase or tenecteplase administration), but subtle early ischemic signs may appear: the Hyperdense MCA sign (a bright white linear attenuation within the horizontal M1 stem of the middle cerebral artery representing an acute intraluminal thromboembolus), loss of the gray-white matter differentiation along the lateral margin of the insula (loss of the insular ribbon sign) and lentiform nucleus, and sulcal effacement from early cytotoxic swelling. Over 12-48 hours, the infarcted vascular territory becomes progressively wedge-shaped and hypodense. When selecting patients for endovascular mechanical thrombectomy between 6 and 24 hours after last known well (DAWN and DEFUSE-3 criteria), CT Angiography (to confirm large-vessel occlusion of the internal carotid or M1/M2 MCA) is paired with CT Perfusion (or MRI DWI/FLAIR mismatch) to quantify the small irreversibly infarcted core relative to the large salvageable ischemic penumbra.

Contrast-enhanced brain MRI differentiates neoplastic, infectious, and demyelinating parenchymal masses. The differential diagnosis for ring-enhancing brain lesions (mnemonic MAGICAL DR: Metastasis, Abscess, Glioblastoma, Infarct subacute, Contusion, AIDS-related Toxoplasmosis vs. Primary CNS Lymphoma, Demyelination, Radiation necrosis) is narrowed by clinical context and diffusion weighting: a pyogenic brain abscess shows intense central restricted diffusion (bright on DWI, dark on ADC) due to viscous purulent fluid within a smooth thin capsule, whereas a necrotic tumor shows central facilitated diffusion unless highly cellular. In an HIV-positive patient with CD4 less than 100 cells/mm3 presenting with multiple ring-enhancing lesions in the basal ganglia, Toxoplasma gondii encephalitis is most common (treated empirically with sulfadiazine + pyrimethamine + leucovorin); if a solitary periventricular ring-enhancing lesion fails to improve after 10-14 days of toxoplasmosis therapy and shows Epstein-Barr virus (EBV) DNA in CSF, the diagnosis is Primary CNS Lymphoma. Glioblastoma (WHO Grade IV astrocytoma) presents as an irregular, centrally necrotic, ring-enhancing intra-axial mass that crosses the corpus callosum into the contralateral hemisphere (butterfly glioma). Conversely, a Meningioma is an extra-axial benign tumor arising from arachnoid cap cells that appears as a homogeneously enhancing, well-circumscribed dural-based mass with a characteristic dural tail sign and occasional psammomatous calcifications.

Colonic volvulus occurs when a redundant, mobile colonic segment twists around its narrow mesenteric vascular pedicle, creating a closed-loop obstruction. Sigmoid volvulus typically affects elderly, institutionalized, or chronically constipated patients (and patients with Chagas megacolon or Parkinson disease); plain abdominal radiography shows a massively dilated, ahaustral loop of sigmoid colon arising from the pelvis in the left lower quadrant and extending toward the right upper quadrant, forming the pathognomonic inverted U-shaped coffee-bean sign (or bent inner-tube sign), while barium/water-soluble enema shows a bird-beak tapering at the rectosigmoid twist. In an uncomplicated sigmoid volvulus without peritoneal signs or perforation, first-line treatment is urgent endoscopic rigid or flexible sigmoidoscopic detorsion and rectal decompression tube placement, followed by elective sigmoid colectomy during the same admission to prevent recurrence. Conversely, Cecal volvulus occurs in younger patients (30-50 years) due to congenital failure of right colonic retroperitoneal fixation; the dilated cecum twists into the mid-abdomen or left upper quadrant with concomitant small bowel dilation, and because endoscopic detorsion rarely succeeds and gangrene risk is high, first-line treatment is surgical right hemicolectomy. In pediatric patients, classic plain radiograph patterns include the Double-Bubble sign (dilated stomach and proximal duodenum with zero distal gas) in congenital duodenal atresia (Down syndrome) or malrotation with midgut volvulus (differentiated emergently via upper GI contrast series showing the ligament of Treitz to the right of the spine and corkscrew duodenum), and Pneumatosis intestinalis (intramural air bubbles) with portal venous gas in neonatal necrotizing enterocolitis.

Contrast-enhanced helical CT of the abdomen and pelvis is the adult diagnostic workhorse for acute nontraumatic abdominal pain. In Acute Appendicitis, CT demonstrates a dilated (greater than 6 mm outer diameter), non-opacifying retrocecal or pelvic appendix with wall thickening, hyperenhancement, periappendiceal mesenteric fat stranding, and often a calcified appendicolith; presence of a walled-off periappendiceal abscess (greater than 3-4 cm) in a stable patient is managed with CT-guided percutaneous drainage and intravenous antibiotics followed by interval appendectomy in 6-8 weeks. In Acute Diverticulitis (left lower quadrant pain, fever, leukocytosis in older adults), CT is the imaging test of choice, demonstrating sigmoid colonic diverticula, segmental colonic wall thickening (greater than 4 mm), pericolic fat stranding, and potential complications (Hinchey I-IV pericolic/pelvic abscess, colovesical fistula presenting with pneumaturia and fecaluria, or free perforation). Colonoscopy is strictly contraindicated during acute diverticulitis due to perforation risk, but MUST be performed 6-8 weeks after resolution to exclude an underlying perforated colorectal malignancy. In Acute Pancreatitis, diagnosis requires 2 of 3 criteria (characteristic epigastric pain radiating to the back, serum lipase/amylase at least 3x upper limit of normal, and imaging findings); CT is not required in the first 48-72 hours if clinical and biochemical criteria are met, unless diagnostic uncertainty exists or the patient fails to improve, in which case contrast-enhanced CT assesses for necrotizing pancreatitis (non-enhancing pancreatic parenchyma), acute peripancreatic fluid collections, or late (greater than 4 weeks) pancreatic pseudocysts and walled-off necrosis.

Malignant bone sarcomas rapidly erode cortex and elevate the periosteum before it can lay down mature bone, generating aggressive periosteal reactions. Osteosarcoma—the most common primary malignant bone tumor in children and adolescents (bimodal peak: ages 10-20 during the adolescent growth spurt, and elderly patients with Paget disease of bone or prior radiation; linked to RB1 and TP53 Li-Fraumeni mutations)—arises in the metaphysis of long bones (most commonly the distal femur and proximal tibia around the knee). Radiographs reveal a mixed lytic-blastic destructive metaphyseal lesion with a Sunburst appearance (spiculated bone formation along Sharpey fibers) and Codman triangle (elevation of the periosteum at the tumor margin). Ewing sarcoma—an aggressive malignant small round blue cell tumor driven by the t(11;22) EWSR1-FLI1 translocation—typically presents in boys aged 5-20 years with localized pain, swelling, fever, and leukocytosis (frequently mimicking acute osteomyelitis) in the diaphysis of long bones (femur, tibia, humerus) or flat pelvic bones, producing a permeative moth-eaten lytic lesion with concentric laminated Onion-skin periosteal reaction. Overall, however, metastatic carcinoma (from breast, prostate, lung, kidney, or thyroid) is far more common than any primary bone sarcoma in adults over 50; prostate cancer classically produces osteoblastic (sclerotic) vertebral metastases, whereas lung, renal, and thyroid cancers and multiple myeloma (punched-out lytic skull/axial lesions with cold bone scans) produce osteolytic lesions.

Joint and axial spine radiographs distinguish degenerative, crystal, seronegative, and metabolic bone disorders. Osteoarthritis demonstrates asymmetric joint space narrowing, subchondral sclerosis (eburnation), subchondral cysts, and marginal osteophytes (Heberden nodes at the DIP joints and Bouchard nodes at the PIP joints, sparing the MCPs). Rheumatoid arthritis demonstrates symmetric periarticular osteopenia, uniform joint space narrowing, and marginal bony erosions at the MCP and PIP joints and ulnar styloid (sparing the DIPs), alongside risk of atlantoaxial (C1-C2) subluxation on flexion-extension cervical spine views. Ankylosing spondylitis (HLA-B27 seronegative spondyloarthropathy) begins with bilateral symmetric sacroiliitis (blurring, erosions, and fusion of the sacroiliac joints) and progresses up the spine via ossification of the outer annulus fibrosus (syndesmophytes), producing the classic Bamboo spine appearance on AP lumbar radiographs. In metabolic bone disease, Osteomalacia (and pediatric Rickets) from severe vitamin D deficiency produces radiolucent pseudofractures (Looser zones or Milkman fractures—transverse radiolucent bands perpendicular to the cortex along the medial femoral neck, pubic rami, and scapula), whereas Paget disease of bone (osteitis deformans) progresses from lytic skull osteoporosis circumscripta to mixed/sclerotic cotton-wool skull appearance, picture-frame vertebrae, and cortical thickening with bowing of long bones.

In a patient presenting with undifferentiated shock, the Rapid Ultrasound in Shock and Hypotension (RUSH) examination categorizes shock etiology (hypovolemic, cardiogenic, obstructive, or distributive) by sequentially interrogating the Pump (heart), the Tank (inferior vena cava, pleural/peritoneal cavities, and lung parenchyma), and the Pipes (abdominal/thoracic aorta and femoral/popliteal deep veins). Interrogating the Pump differentiates cardiogenic shock (globally depressed left ventricular ejection fraction with minimal anterior mitral leaflet excursion toward the interventricular septum, i.e., elevated E-point septal separation greater than 7 mm), hyperdynamic left ventricular function (walls kissing at end-systole, seen in hypovolemic or early septic distributive shock), acute massive pulmonary embolism (severely dilated right ventricle exceeding left ventricular size, interventricular septal flattening creating a D-shaped left ventricle on parasternal short-axis view, and McConnell sign—akinesia of the mid-free RV wall with preserved apical contractility), and Cardiac Tamponade (circumferential pericardial effusion accompanied by diastolic collapse of the right ventricle and systolic collapse of the right atrium). Interrogating the Tank via the subxiphoid IVC view correlates directly with central venous pressure: a small IVC (less than 1.5 cm) collapsing greater than 50% with inspiration confirms low right atrial pressure (hypovolemic or distributive shock responsive to IV fluid boluses), whereas a plethora-dilated IVC (greater than 2.1 cm) with less than 50% inspiratory collapse confirms elevated right atrial pressure (cardiogenic or obstructive shock from tamponade, tension pneumothorax, or massive PE).

In acute dyspnea (the BLUE protocol), thoracic POCUS differentiates acute decompensated heart failure from COPD/asthma exacerbation in seconds. Vertical, laser-like hyperechoic reverberation artifacts arising from the pleural line, extending to the bottom of the screen without fading, obliterating A-lines, and moving synchronously with lung sliding are termed B-lines (lung rockets). The presence of 3 or more B-lines per intercostal space bilaterally across anterior and lateral chest zones confirms diffuse interstitial alveolar-capillary syndrome (cardiogenic pulmonary edema or ARDS) with greater than 95% sensitivity, whereas a predominating A-line profile with preserved lung sliding rules out pulmonary edema and points toward COPD/asthma or pulmonary embolism. To evaluate the Pipes in suspected thromboembolism or abdominal pain, bedside aortic ultrasound scans the abdominal aorta from the celiac trunk to the iliac bifurcation in transverse plane measuring outer-wall to outer-wall diameter (greater than 3.0 cm defines an abdominal aortic aneurysm; greater than 5.0-5.5 cm with hypotension indicates ruptured AAA). Finally, 2-point (or 3-point) lower extremity DVT compression ultrasound uses a high-frequency linear transducer to apply firm downward compression over the common femoral vein at the saphenofemoral junction and the popliteal vein in the popliteal fossa: a normal vein collapses completely until its anterior and posterior walls touch, whereas non-compressibility of the venous lumen is diagnostic of acute Deep Vein Thrombosis.