Spotters Set 23 (FREE ACCESS)

1. Retroperitoneal lymphoma. OSCE Questions

   • Clinical: Middle-aged to older adults; male predominance; abdominal pain, weight loss, palpable mass; B symptoms less common; may present with obstructive symptoms from mass effect

   • Etiology/Pathophys: Non-Hodgkin lymphoma arising in retroperitoneal lymph nodes or extranodal sites; DLBCL most common subtype; can be primary retroperitoneal or secondary involvement

   • CT: Large soft tissue mass (mean 7-12cm); homogeneous hypoenhancement relative to muscle; encasement of major vessels without stenosis/occlusion; minimal necrosis; may show peripancreatic lymphadenopathy

   • MRI: T1 hypointense, T2 hyperintense mass; homogeneous enhancement pattern; excellent soft tissue contrast for vessel relationship assessment

   • Frameworks: Ann Arbor staging system; Stage I (single node region), Stage II (≥2 node regions same side of diaphragm), Stage III (nodes both sides diaphragm), Stage IV (extranodal)

   • DDx: Sarcoma (more heterogeneous, frequent necrosis, older age); metastases (known primary, multiple lesions); infection/abscess (fever, rim enhancement); desmoid tumor (younger patients, infiltrative)

   • Tx: Chemotherapy primary treatment (R-CHOP for DLBCL); surgery contraindicated as lymphoma is chemosensitive; core needle biopsy for tissue diagnosis; excellent response to systemic therapy

2. Right iliopsoas intramuscular lipoma. OSCE Questions

   • Clinical: 40-60y; M=F; usually asymptomatic or mild hip/groin discomfort; can cause mass effect with hip flexion weakness; rare infiltrating lipoma subtype

   • Etiology/Pathophys: Benign mesenchymal tumor composed of mature adipocytes infiltrating between muscle fibers; tends to have infiltrative growth pattern unlike superficial lipomas

   • CT: Homogeneous fat density (-50 to -150 HU) mass within iliopsoas muscle; may contain thin fibrous septations; infiltrative margins with muscle fiber interdigitation

   • MRI: Follows fat signal on all sequences (T1 hyperintense, T2 hyperintense, fat-suppressed sequences hypointense); thin internal septations may enhance; infiltrative borders with finger-like projections between muscle bundles

   • DDx: Well-differentiated liposarcoma (thick irregular septations >2mm, nodular non-fat components); muscle herniation (continuity with muscle belly); chronic hematoma (hemosiderin, different signal characteristics)

   • Tx: Surgical excision if symptomatic or diagnostic uncertainty; wide margins recommended due to infiltrative nature; recurrence rate 50-80% with incomplete excision

3. Muscular dystrophy. OSCE Questions

   • Clinical: Boys (X-linked DMD) or both sexes (LGMD, CMD); onset birth to childhood; progressive muscle weakness; pseudohypertrophy; cardiomyopathy; respiratory compromise; Gower sign; elevated CK; steroid-responsive in DMD

   • Etiology/Pathophys: Dystrophin gene mutations (DMD); FKRP, LAMA2 mutations (CMD/LGMD); progressive muscle fiber degeneration → fatty infiltration → fibrosis; cardiac involvement via similar mechanism

   • MRI: Increased T2 signal in affected muscles; fatty infiltration on T1WI; gluteus maximus most severely affected in DMD; symmetric proximal > distal involvement; cardiac fibrosis on LGE; brain abnormalities in CMD (white matter hyperintensities, cortical dysplasia, cobblestone malformation)

   • Frameworks: Mercuri scale (0-4 grading of fatty infiltration); T2 mapping for quantitative disease monitoring; cardiac MRI strain analysis for fibrosis detection

   • DDx: Immune-mediated necrotizing myopathy (more inflammatory, asymmetric); spinal muscular atrophy (anterior horn cell disease); metabolic myopathy (glycogen storage diseases); inflammatory myositis (enhancement, edema)

   • Tx: Corticosteroids (deflazacort, prednisone); cardiac monitoring and ACE inhibitors; vitamin D supplementation; respiratory support; genetic counseling; physical therapy

4. Anterior Nutcracker syndrome: Left renal vein compressed between SMA and Aorta. What is posterior nutcracker syndrome? Let me know in the comments section! OSCE Questions

   • Clinical: Adults 30s-60s; M=F; left flank pain; hematuria; varicocele; may present with diffuse abdominal pain

   • Etiology/Pathophys: Retro-aortic left renal vein (anatomic variant) becomes compressed between aorta anteriorly and vertebral body posteriorly → increased left renal venous pressure → symptoms

   • CT: Retro-aortic left renal vein compressed between aorta and anterior margin of L1 vertebral body; proximal LRV dilatation; multiple venous collaterals draining to hemiazygos vein and IVC; dilated left gonadal vein

   • DDx: Anterior nutcracker syndrome (LRV compression between SMA and aorta – more common); May-Thurner syndrome (left common iliac vein compression); can cause pelvic congestion syndrome in women

   • Tx: Conservative management for asymptomatic cases; surgical intervention for symptomatic patients; endovascular percutaneous intervention for associated pelvic congestion; open surgical repair preferred treatment modality

5. Perineural / Tarlov cyst. OSCE Questions

   • Clinical: 40-60y; F>M (3:1); asymptomatic in 80% of cases; symptomatic cases present with radicular pain, numbness, weakness; sacral location most common; etymology – named after Isadore Tarlov who first described them

   • Etiology/Pathophys: Developmental outpouching of nerve root sheaths; contain CSF and nerve root fibers; may enlarge due to ball-valve mechanism of CSF flow; can cause bony erosion when large

   • CT: Well-defined, thin-walled, fluid-density lesions in neural foramina; sacral location most common (S2-S3); may show bony erosion or neural foraminal expansion; multiple cysts common

   • MRI: CSF signal intensity on all sequences (T1 hypointense, T2 hyperintense, FLAIR hypointense); thin rim enhancement; nerve root may be seen traversing the cyst; sacral predominance; communicates with thecal sac

   • Signs: Communicating cyst sign – direct communication with thecal sac differentiates from other cystic lesions; nerve root sign – nerve root visible within or adjacent to cyst

   • DDx: Synovial cyst (facet joint origin, non-communicating); arachnoid cyst (usually thoracic, broader-based); schwannoma (enhancing nodule); meningocele (broader communication)

   • Tx: Conservative management for asymptomatic; percutaneous aspiration, fibrin glue injection, or surgical fenestration for symptomatic cases; avoid simple aspiration alone due to high recurrence

6. Left ureterocele. OSCE Questions

   • Clinical: Most common in infants and children; F>M; may present with UTIs, urinary retention, incontinence, abdominal pain; simple ureteroceles in adults, ectopic ureteroceles in children with duplex systems

   • Etiology/Pathophys: Cystic dilatation of terminal ureter within bladder; failure of normal regression of Chwalla membrane; associated with duplex collecting systems and upper pole moiety

   • US: Thin-walled cystic structure within bladder; may show comet tail artifact; associated hydronephrosis of affected moiety; best seen when bladder distended

   • CT: Hypodense cystic lesion projecting into bladder lumen; cobra head sign on excretory phase; may show delayed excretion from affected kidney; CTU helpful for surgical planning

   • MRI: T2 hyperintense cystic lesion in bladder; T1 hypointense; excellent for evaluating duplex systems and associated anomalies

   • Frameworks: Simple (intravesical, single system) vs Ectopic (extends beyond bladder neck, duplex system); Cecoureterocele classification based on location and associated anomalies

   • DDx: Bladder diverticulum (wider neck), pseudoureterocele (edema around ureteral orifice), bladder tumor, multicystic dysplastic kidney in pelvis

   • Tx: Small asymptomatic cases may be observed; endoscopic incision for simple cases; ureteroneocystostomy or upper pole heminephrectomy for complex ectopic cases

7. Crohn’s disease with enteropathic sacroiliitis. OSCE Questions

   • Clinical: Young adults with IBD (mean age 14.3y); equal M:F distribution; often asymptomatic for musculoskeletal symptoms; Crohn’s disease more common than UC; arthritis can occur before, during, or after IBD diagnosis

   • Etiology/Pathophys: Extraintestinal manifestation of IBD; shared genetic, immunological, and clinical features between spondyloarthritis and IBD; chronic inflammatory process affecting sacroiliac joints

   • MRI: Bone marrow edema on T2W fat-suppressed sequences; diffusion restriction on DWI/DWIBS; dynamic contrast enhancement in affected SI joints; findings typically mild degree; gadolinium enhancement does not improve diagnostic specificity

   • Frameworks: ASAS criteria used for sacroiliitis assessment; SI joints divided into 4 quadrants (upper/lower iliac, upper/lower sacral); peripheral SpA (41.1%), axial SpA (32.1%), mixed pattern (26.8%)

   • DDx: Other spondyloarthropathies; ankylosing spondylitis; psoriatic arthritis; reactive arthritis; infectious sacroiliitis

   • Tx: NSAIDs and corticosteroids; conventional synthetic DMARDs (methotrexate most common); biological DMARDs (anti-TNF agents most used); multidisciplinary care with gastroenterology

8. Left renal angiomyolipoma with an aneurysm. OSCE Questions

   • Clinical: Wide age range (13-41y); F>M; flank pain; hematuria; palpable mass; associated with tuberous sclerosis (45-80% cases); risk of Wunderlich syndrome (acute flank pain, flank mass, hypovolemic shock from retroperitoneal hemorrhage)

   • Etiology/Pathophys: Benign tumor from perivascular epitheloid cells; composed of fat tissue, smooth muscle, abnormal blood vessels; aneurysms develop in dysplastic vessels; aneurysm size correlates with rupture risk; estrogen/androgen receptor positive

   • US: Hyperechoic mass with posterior acoustic shadowing; pseudoaneurysm may be visible on color Doppler; heterogeneous echotexture

   • CT: Fat density (-20 to -80 HU); aneurysmal dilatation in 50% of cases; multiple enhancing vessels; perirenal fat stranding if hemorrhage; retroperitoneal hematoma if ruptured; pseudoaneurysm enhancement

   • MRI: Fat signal on T1WI; pseudoaneurysm with flow voids; useful in pregnancy to avoid radiation; can demonstrate extent of retroperitoneal hemorrhage

   • Signs: Wunderlich syndrome (Lenk’s triad: acute flank pain, flank mass, hypovolemic shock); fat-containing renal mass with vascular aneurysm

   • DDx: Renal cell carcinoma with necrosis (no macroscopic fat); retroperitoneal liposarcoma (exophytic cases); fat-poor AML (no fat density); bleeding renal cyst

   • Tx: Selective arterial embolization for bleeding aneurysms (microparticles/coils); conservative management if asymptomatic; partial nephrectomy for large/symptomatic lesions; prophylactic embolization for aneurysms >5mm

9. Stercoral colitis. OSCE Questions

   • Clinical: Elderly patients (mean age 77y); no gender predisposition; acute abdominal pain, bloating, changes in bowel habits; chronic constipation, systemic medical diseases, anticholinergic drugs; etymology from Latin “stercoral” meaning “related to feces”

   • Etiology/Pathophys: Hard stool masses (fecalomas) accumulate in colon causing persistent pressure on colonic wall → localized inflammation, irritation, and potential necrosis of colonic mucosa

   • CT: Pericolonic stranding (80%, most sensitive); perfusion defects (70%); dense mucosa (62.5%); colon wall thickening (60%); abnormal gas (50%) with pneumo-mesocolon (40%); proximal colon dilatation (20%); pericolonic abscess (20%); mucosal sloughing (10%); ascites in fatal cases

   • Signs: Dense mucosa sign (71% sensitivity, 86% specificity for fatal cases); perfusion defect sign (75% sensitivity, 79% specificity); mucosal sloughing and pericolonic abscess have high specificity (100% and 93%) for fatal stercoral colitis

   • DDx: Acute mesenteric ischemia (similar abdominal pain but lacks fecal impaction); acute appendicitis (especially in elderly with anticholinergic use); benign stool impaction (lacks inflammatory CT changes)

   • Tx: Bowel evacuation and disimpaction; addressing underlying fecal impaction; surgical intervention may be required for necrotic or perforated cases

10. Right portal vein thrombosis with Transient Hepatic Attenuation Defect (THAD). OSCE Questions

    • Clinical: All ages; often asymptomatic; may present with abdominal pain, fever, or symptoms related to underlying cause; risk factors include cirrhosis, liver malignancy, local inflammatory conditions, thrombophilic diseases, trauma, umbilical catheterization in neonates

    • Etiology/Pathophys: Portal vein thrombosis causes decreased portal venous flow to affected hepatic segment; compensatory increased hepatic arterial flow creates perfusion mismatch; THAD represents geographic area of altered perfusion due to dual blood supply disruption

    • CT: Right portal vein filling defect with lack of enhancement; THAD appears as geographic, wedge-shaped area of decreased attenuation in arterial phase involving right hepatic lobe; enhancement normalizes on delayed phases; may show collateral circulation formation

    • Signs: THAD sign – transient hepatic attenuation difference on arterial phase CT corresponding to portal vein distribution territory

    • DDx: Hepatic infarction (persistent hypoenhancement), focal fatty infiltration (no vascular correlation), hepatic arterial thrombosis (persistent decreased enhancement), tumor (mass effect, different enhancement pattern)

    • Tx: Anticoagulation therapy for acute thrombosis; treatment of underlying cause; drainage if associated with abscess; long-term monitoring for portal hypertension development

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